start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=519
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250926
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Specific induction of right ventricular-like cardiomyocytes from human pluripotent stem cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Applications employing human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) require well-characterized, chamber-specific hPSC-CMs. Distinct first heart field (FHF) and second heart field (SHF) cardiac progenitor populations give rise to the left ventricular (LV) and right ventricular (RV) cardiomyocytes, respectively. This developmental difference in cardiomyocyte origin suggests that chamber-specific cardiomyocytes have unique characteristics. Therefore, efficient strategies to differentiate human pluripotent stem cells (hPSCs) specifically to LV-like or RV-like cardiomyocytes are needed and it is still unknown whether there is a phenotypic difference between LV-like cardiomyocytes and RV-like cardiomyocytes derived from hPSCs.<br>
Methods An established hPSC cardiac differentiation protocol employing sequential GSK3β inhibition followed by Wnt inhibition (GiWi) was modified by addition of insulin or BMP antagonists during mesoderm formation. Cardiac progenitor populations were evaluated for FHF and SHF markers, and differentiated hPSC-CMs were characterized for chamber-specific markers.<br>
Results The GiWi protocol produced mainly FHF-like progenitor cells that gave rise to LV-like cardiomyocytes. Inhibition of endogenous BMP signaling during mesoderm induction using insulin or BMP antagonists reduced expression of FHF markers and increased expression of SHF markers in cardiac progenitor cells. hPSC-CMs arising from the SHF-like progenitor cells showed an RV-like gene expression pattern and exhibited phenotypic differences in spontaneous contraction rate, Ca2+ transients, and cell size compared to control LV-like cardiomyocytes.<br>
Conclusion This study establishes methodology to generate RV-like hPSC-CMs to support the development of disease modeling research using chamber-specific hPSC-CMs.
en-copyright=
kn-copyright=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KatanosakaYuki
en-aut-sei=Katanosaka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IidaToshihiro
en-aut-sei=Iida
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KusumotoDai
en-aut-sei=Kusumoto
en-aut-mei=Dai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SatoRyushi
en-aut-sei=Sato
en-aut-mei=Ryushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AdachiRiki
en-aut-sei=Adachi
en-aut-mei=Riki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ShimizuSatoshi
en-aut-sei=Shimizu
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KurokawaJunko
en-aut-sei=Kurokawa
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NishidaMikako
en-aut-sei=Nishida
en-aut-mei=Mikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=UdonoHeiichiro
en-aut-sei=Udono
en-aut-mei=Heiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=ZhangJianhua
en-aut-sei=Zhang
en-aut-mei=Jianhua
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=YuasaShinsuke
en-aut-sei=Yuasa
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=KampTimothy J.
en-aut-sei=Kamp
en-aut-mei=Timothy J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Physiology, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Biomedical Informatics and Molecular Biology, The Sakaguchi Laboratory, Keio University School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Bio-Informational Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka
kn-affil=

affil-num=7
en-affil=Department of Bio-Informational Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka
kn-affil=

affil-num=8
en-affil=Department of Bio-Informational Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka
kn-affil=

affil-num=9
en-affil=Department of Bio-Informational Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Therapeutics, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Physiology, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Metabolic Immune Regulation, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Metabolic Immune Regulation, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=17
en-affil=Department of Medicine, University of Wisconsin School of Medicine and Public Health
kn-affil=

affil-num=18
en-affil=Department of Cardiovascular Medicine, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=19
en-affil=Department of Medicine, University of Wisconsin School of Medicine and Public Health
kn-affil=

affil-num=20
en-affil=Department of Cardiovascular Medicine, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Human pluripotent stem cell-derived cardiomyocytes
kn-keyword=Human pluripotent stem cell-derived cardiomyocytes
en-keyword=Anterior second heart field
kn-keyword=Anterior second heart field
en-keyword=Right ventricle
kn-keyword=Right ventricle
en-keyword=Bone morphogenetic protein
kn-keyword=Bone morphogenetic protein
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=3
article-no=
start-page=412
end-page=437
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250908
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Biophysical regulation of extracellular matrix in systemic lupus erythematosus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Systemic lupus erythematosus (SLE) is a prototypical autoimmune disease characterized by immune dysregulation and multi-organ damage. Recent advances have underscored the critical involvement of extracellular matrix (ECM) biophysical properties in shaping immune cell behavior and metabolic states that contribute to disease progression. This review systematically delineates the pathological remodeling of ECM biophysics in SLE, with a focus on their roles in mechanotransduction, immune-metabolic interplay, and organ-specific tissue injury. By integrating current evidence, we highlight how ECM-derived mechanical cues orchestrate aberrant immune responses and propose new perspectives for targeting ECM-immune crosstalk in the development of organ-specific, mechanism-based therapies for SLE.
en-copyright=
kn-copyright=

en-aut-name=LiQiwei
en-aut-sei=Li
en-aut-mei=Qiwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=LiQiang
en-aut-sei=Li
en-aut-mei=Qiang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=XiaoZhaoyang
en-aut-sei=Xiao
en-aut-mei=Zhaoyang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NARUSEKeiji
en-aut-sei=NARUSE
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Anesthesiology, The Second Affiliated Hospital of Dalian Medical University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=systemic lupus erythematosus (SLE)
kn-keyword=systemic lupus erythematosus (SLE)
en-keyword=extracellular matrix (ECM)
kn-keyword=extracellular matrix (ECM)
en-keyword=mechanotransduction
kn-keyword=mechanotransduction
en-keyword=mechanism
kn-keyword=mechanism
en-keyword=immune regulation
kn-keyword=immune regulation
en-keyword=fibrosis
kn-keyword=fibrosis
en-keyword=organ-specific damage
kn-keyword=organ-specific damage
END

start-ver=1.4
cd-journal=joma
no-vol=137
cd-vols=
no-issue=2
article-no=
start-page=80
end-page=81
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Anatomy-Physiology-Pharmacology Week in 2025
kn-title=第130回日本解剖学会／第102回日本生理学会／第98回日本薬理学会合同大会
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=成瀬恵治
kn-aut-sei=成瀬
kn-aut-mei=恵治
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学学術研究院医歯薬学域　システム生理学
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=30648
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250820
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of mechanical stretching stimulation on maturation of human iPS cell-derived cardiomyocytes co-cultured with human gingival fibroblasts
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In the realm of regenerative medicine, despite the various techniques available for inducing the differentiation of induced pluripotent stem (iPS) cells into cardiomyocytes, there remains a need to enhance the maturation of the cardiomyocytes. This study aimed to improve the differentiation and subsequent maturation of iPS-derived cardiomyocytes (iPS-CMs) by incorporating mechanical stretching. Human iPS cells were co-cultured with human gingival fibroblasts (HGF) on a polydimethylsiloxane (PDMS) stretch chamber, where mechanical stretching stimulation was applied during the induction of cardiomyocyte differentiation. The maturation of iPS-CMs was assessed using qRT-PCR, immunocytochemistry, transmission electron microscopy, calcium imaging and contractility comparisons. Results indicated significantly elevated gene expression levels of cardiomyocyte markers (cTnT) and the mesodermal marker (Nkx2.5) in the stretch group compared to the control group. Fluorescent immunocytochemical staining revealed the presence of cardiac marker proteins (cTnT and MYL2) in both groups, with higher protein expression in the stretch group. Additionally, structural maturation of iPS-CMs in the stretch group was notably better than in the control group. A significant increase in the contractility and calcium cycle of iPS-CMs was observed in the stretch group. These findings demonstrate that mechanical stretching stimulation enhances the maturation of iPS-CMs co-cultured with HGF.
en-copyright=
kn-copyright=

en-aut-name=WangMengxue
en-aut-sei=Wang
en-aut-mei=Mengxue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IdeiHarumi
en-aut-sei=Idei
en-aut-mei=Harumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangChen
en-aut-sei=Wang
en-aut-mei=Chen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=LiangYin
en-aut-sei=Liang
en-aut-mei=Yin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=LiuYun
en-aut-sei=Liu
en-aut-mei=Yun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsudaYusuke
en-aut-sei=Matsuda
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KamiokaHiroshi
en-aut-sei=Kamioka
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Nursing, School of Life and Health Sciences, HuZhou College
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Human induced pluripotent stem cell
kn-keyword=Human induced pluripotent stem cell
en-keyword=Cardiomyocyte
kn-keyword=Cardiomyocyte
en-keyword=Human gingival fibroblast
kn-keyword=Human gingival fibroblast
en-keyword=Mechanical stretching
kn-keyword=Mechanical stretching
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=30648
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250820
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of mechanical stretching stimulation on maturation of human iPS cell-derived cardiomyocytes co-cultured with human gingival fibroblasts
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In the realm of regenerative medicine, despite the various techniques available for inducing the differentiation of induced pluripotent stem (iPS) cells into cardiomyocytes, there remains a need to enhance the maturation of the cardiomyocytes. This study aimed to improve the differentiation and subsequent maturation of iPS-derived cardiomyocytes (iPS-CMs) by incorporating mechanical stretching. Human iPS cells were co-cultured with human gingival fibroblasts (HGF) on a polydimethylsiloxane (PDMS) stretch chamber, where mechanical stretching stimulation was applied during the induction of cardiomyocyte differentiation. The maturation of iPS-CMs was assessed using qRT-PCR, immunocytochemistry, transmission electron microscopy, calcium imaging and contractility comparisons. Results indicated significantly elevated gene expression levels of cardiomyocyte markers (cTnT) and the mesodermal marker (Nkx2.5) in the stretch group compared to the control group. Fluorescent immunocytochemical staining revealed the presence of cardiac marker proteins (cTnT and MYL2) in both groups, with higher protein expression in the stretch group. Additionally, structural maturation of iPS-CMs in the stretch group was notably better than in the control group. A significant increase in the contractility and calcium cycle of iPS-CMs was observed in the stretch group. These findings demonstrate that mechanical stretching stimulation enhances the maturation of iPS-CMs co-cultured with HGF.
en-copyright=
kn-copyright=

en-aut-name=WangMengxue
en-aut-sei=Wang
en-aut-mei=Mengxue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IdeiHarumi
en-aut-sei=Idei
en-aut-mei=Harumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangChen
en-aut-sei=Wang
en-aut-mei=Chen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=LiangYin
en-aut-sei=Liang
en-aut-mei=Yin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=LiuYun
en-aut-sei=Liu
en-aut-mei=Yun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsudaYusuke
en-aut-sei=Matsuda
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KamiokaHiroshi
en-aut-sei=Kamioka
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Nursing, School of Life and Health Sciences, HuZhou College
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Human induced pluripotent stem cell
kn-keyword=Human induced pluripotent stem cell
en-keyword=Cardiomyocyte
kn-keyword=Cardiomyocyte
en-keyword=Human gingival fibroblast
kn-keyword=Human gingival fibroblast
en-keyword=Mechanical stretching
kn-keyword=Mechanical stretching
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=1
article-no=
start-page=715
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250508
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=TRPV2 mediates stress resilience in mouse cardiomyocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The heart dynamically compensates for haemodynamic stress, but how this resilience forms during cardiac growth is not clear. Using a temporally inducible, cardiac-specific knockout in mice we show that the Transient receptor potential vanilloid family 2 (TRPV2) channel is crucial for the maturation of cardiomyocyte stress resilience. TRPV2 defects in growing hearts lead to small morphology, abnormal intercalated discs, weak contractility, and low expression of serum response factor and Insulin-like growth factor-1 (IGF-1) signalling. Individual cardiomyocytes of TRPV2-deficient hearts show reduced contractility with abnormal Ca2+ handling. In cultured neonatal cardiomyocytes, mechanical Ca2+ response, excitation-contraction coupling, sarcoplasmic reticulum Ca2+ content, actin formation, nuclear localisation of Myocyte enhancer factor 2c, and IGF-1 expression require TRPV2. TRPV2-deficient hearts show a defective response to dobutamine stress and no compensatory hypertrophic response to phenylephrine administration, but no stress response to pressure overload. These data suggest TRPV2 mediates the maturation of cardiomyocyte stress resilience, and will advance therapeutic interventions and drug discovery for heart disease.
en-copyright=
kn-copyright=

en-aut-name=DongYubing
en-aut-sei=Dong
en-aut-mei=Yubing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangGuohao
en-aut-sei=Wang
en-aut-mei=Guohao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UjiharaYoshihiro
en-aut-sei=Ujihara
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ChenYanzhu
en-aut-sei=Chen
en-aut-mei=Yanzhu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KatanosakaKimiaki
en-aut-sei=Katanosaka
en-aut-mei=Kimiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KatanosakaYuki
en-aut-sei=Katanosaka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Electrical and Mechanical Engineering, Graduate School of Engineering, Nagoya Institute of Technology
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Biomedical Sciences, College of Life and Health Sciences, Chubu University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=16
article-no=
start-page=1373
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240817
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Direct Binding of Synaptopodin 2-Like Protein to Alpha-Actinin Contributes to Actin Bundle Formation in Cardiomyocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Synaptopodin 2-like protein (SYNPO2L) is localized in the sarcomere of cardiomyocytes and is involved in heart morphogenesis. However, the molecular function of SYNPO2L in the heart is not fully understood. We investigated the interaction of SYNPO2L with sarcomeric alpha-actinin and actin filaments in cultured mouse cardiomyocytes. Immunofluorescence studies showed that SYNPO2L colocalized with alpha-actinin and actin filaments at the Z-discs of the sarcomere. Recombinant SYNPO2La or SYNPO2Lb caused a bundling of the actin filaments in the absence of alpha-actinin and enhanced the alpha-actinin-dependent formation of actin bundles. In addition, high-speed atomic force microscopy revealed that SYNPO2La directly bound to alpha-actinin via its globular ends. The interaction between alpha-actinin and SYNPO2La fixed the movements of the two proteins on the actin filaments. These results strongly suggest that SYNPO2L cooperates with alpha-actinin during actin bundle formation to facilitate sarcomere formation and maintenance.
en-copyright=
kn-copyright=

en-aut-name=YamadaHiroshi
en-aut-sei=Yamada
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OsakaHirona
en-aut-sei=Osaka
en-aut-mei=Hirona
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TatsumiNanami
en-aut-sei=Tatsumi
en-aut-mei=Nanami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ArakiMiu
en-aut-sei=Araki
en-aut-mei=Miu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AbeTadashi
en-aut-sei=Abe
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KaiharaKeiko
en-aut-sei=Kaihara
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakashimaEizo
en-aut-sei=Takashima
en-aut-mei=Eizo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UchihashiTakayuki
en-aut-sei=Uchihashi
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakeiKohji
en-aut-sei=Takei
en-aut-mei=Kohji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Neuroscience, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Science, Nagoya University
kn-affil=

affil-num=3
en-affil=Department of Neuroscience, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Neuroscience, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neuroscience, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Division of Malaria Research, Proteo-Science Center, Ehime University
kn-affil=

affil-num=9
en-affil=Graduate School of Science, Nagoya University
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Neuroscience, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=SYNPO2L
kn-keyword=SYNPO2L
en-keyword=actinin
kn-keyword=actinin
en-keyword=actin
kn-keyword=actin
en-keyword=sarcomere
kn-keyword=sarcomere
en-keyword=cardiomyocyte
kn-keyword=cardiomyocyte
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=18063
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240808
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Human heart-on-a-chip microphysiological system comprising endothelial cells, fibroblasts, and iPSC-derived cardiomyocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In recent years, research on organ-on-a-chip technology has been flourishing, particularly for drug screening and disease model development. Fibroblasts and vascular endothelial cells engage in crosstalk through paracrine signaling and direct cell-cell contact, which is essential for the normal development and function of the heart. Therefore, to faithfully recapitulate cardiac function, it is imperative to incorporate fibroblasts and vascular endothelial cells into a heart-on-a-chip model. Here, we report the development of a human heart-on-a-chip composed of induced pluripotent stem cell (iPSC)-derived cardiomyocytes, fibroblasts, and vascular endothelial cells. Vascular endothelial cells cultured on microfluidic channels responded to the flow of culture medium mimicking blood flow by orienting themselves parallel to the flow direction, akin to in vivo vascular alignment in response to blood flow. Furthermore, the flow of culture medium promoted integrity among vascular endothelial cells, as evidenced by CD31 staining and lower apparent permeability. The tri-culture condition of iPSC-derived cardiomyocytes, fibroblasts, and vascular endothelial cells resulted in higher expression of the ventricular cardiomyocyte marker IRX4 and increased contractility compared to the bi-culture condition with iPSC-derived cardiomyocytes and fibroblasts alone. Such tri-culture-derived cardiac tissues exhibited cardiac responses similar to in vivo hearts, including an increase in heart rate upon noradrenaline administration. In summary, we have achieved the development of a heart-on-a-chip composed of cardiomyocytes, fibroblasts, and vascular endothelial cells that mimics in vivo cardiac behavior.
en-copyright=
kn-copyright=

en-aut-name=LiuYun
en-aut-sei=Liu
en-aut-mei=Yun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KamranRumaisa
en-aut-sei=Kamran
en-aut-mei=Rumaisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HanXiaoxia
en-aut-sei=Han
en-aut-mei=Xiaoxia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangMengxue
en-aut-sei=Wang
en-aut-mei=Mengxue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=LiQiang
en-aut-sei=Li
en-aut-mei=Qiang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=LaiDaoyue
en-aut-sei=Lai
en-aut-mei=Daoyue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Induced pluripotent stem cells
kn-keyword=Induced pluripotent stem cells
en-keyword=Fibroblasts
kn-keyword=Fibroblasts
en-keyword=Endothelial cells
kn-keyword=Endothelial cells
en-keyword=Heart
kn-keyword=Heart
en-keyword=Heart-on-a-chip
kn-keyword=Heart-on-a-chip
en-keyword=Organ-on-a-chip
kn-keyword=Organ-on-a-chip
END

start-ver=1.4
cd-journal=joma
no-vol=121
cd-vols=
no-issue=17
article-no=
start-page=3286
end-page=3294
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220906
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=High hydrostatic pressure induces slow contraction in mouse cardiomyocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cardiomyocytes are contractile cells that regulate heart contraction. Ca2+ flux via Ca2+ channels activates actomyosin interactions, leading to cardiomyocyte contraction, which is modulated by physical factors (e.g., stretch, shear stress, and hydrostatic pressure). We evaluated the mechanism triggering slow contractions using a high-pressure microscope to characterize changes in cell morphology and intracellular Ca2+ concentration ([Ca2+]i) in mouse cardiomyocytes exposed to high hydrostatic pressures. We found that cardiomyocytes contracted slowly without an acute transient increase in [Ca2+]i, while a myosin ATPase inhibitor interrupted pressure-induced slow contractions. Furthermore, transmission electron microscopy showed that, although the sarcomere length was shortened upon the application of 20 MPa, this pressure did not collapse cellular structures such as the sarcolemma and sarcomeres. Our results suggest that pressure-induced slow contractions in cardiomyocytes are driven by the activation of actomyosin interactions without an acute transient increase in [Ca2+]i.
en-copyright=
kn-copyright=

en-aut-name=YamaguchiYohei
en-aut-sei=Yamaguchi
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiyamaMasayoshi
en-aut-sei=Nishiyama
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KaiHiroaki
en-aut-sei=Kai
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KanekoToshiyuki
en-aut-sei=Kaneko
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KaiharaKeiko
en-aut-sei=Kaihara
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IribeGentaro
en-aut-sei=Iribe
en-aut-mei=Gentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakaiAkira
en-aut-sei=Takai
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MorimatsuMasatoshi
en-aut-sei=Morimatsu
en-aut-mei=Masatoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Physics, Faculty of Science and Engineering, Kindai University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Physiology, Asahikawa Medical University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Physiology, Asahikawa Medical University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=
article-no=
start-page=101404
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=2021
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Production of TRPM4 knockout cell line using rat cardiomyocyte H9c2
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The method presented in this article are related to the research article entitled as "Role of the TRPM4 channel in mitochondrial function, calcium release, and ROS generation in oxidative stress" [1]. TRPM4, a non-selective monovalent cation channel, is not only involved in the generation of the action potential in cardiomyocytes, but also thought to be a key molecule in the development of the ischemia-reperfusion injury of the brain and the heart [2-5]. However, existing pharmacological inhibitors for the TRPM4 channel have problems of non-specificity [6]. This article describes methods used for targeted genomic deletion in the rat cardiomyocyte H9c2 using the CRISPR-Cas9 genome editing system in order to suppress TRPM4 protein expression. Confocal microscopy, flow cytometry, Sanger sequencing, and western blotting are performed to confirm vector transfection and the subsequent knockout of the TRPM4 protein. These data provide information on the comprehensive analyses for knocking out the rat TRPM4 channel using CRISPR/Cas9. The analyses include confocal microscopy, flow cytometry, Sanger sequencing, and western blotting. This dataset will benefit biological and medical researchers studying the function of TRPM4-expressing cells including neurons, cardiomyocytes, and vascular endothelial cells. It is also useful to study the involvement of the TRPM4 channel in pathological processes such as cardiac arrhythmia and ischemia-reperfusion injury. The dataset can be used to guide the experiment of knocking out the TRPM4 gene and its subsequent application to the study of disease process caused by the gene. 
en-copyright=
kn-copyright=

en-aut-name=WangChen
en-aut-sei=Wang
en-aut-mei=Chen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MaedaMasakazu
en-aut-sei=Maeda
en-aut-mei=Masakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ChenJian
en-aut-sei=Chen
en-aut-mei=Jian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangMengxue
en-aut-sei=Wang
en-aut-mei=Mengxue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medicine, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=TRPM4
kn-keyword=TRPM4
en-keyword=Cardiomyocyte
kn-keyword=Cardiomyocyte
en-keyword=H9c2
kn-keyword=H9c2
en-keyword=CRISPR/Cas9
kn-keyword=CRISPR/Cas9
en-keyword=Confocal microscopy
kn-keyword=Confocal microscopy
en-keyword=DNA sequencing
kn-keyword=DNA sequencing
en-keyword=Flow cytometry
kn-keyword=Flow cytometry
en-keyword=Western blotting
kn-keyword=Western blotting
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=
article-no=
start-page=689662
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210804
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Meta-Analysis-Assisted Detection of Gravity-Sensitive Genes in Human Vascular Endothelial Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Gravity affects the function and maintenance of organs, such as bones, muscles, and the heart. Several studies have used DNA microarrays to identify genes with altered expressions in response to gravity. However, it is technically challenging to combine the results from various microarray datasets because of their different data structures. We hypothesized that it is possible to identify common changes in gene expression from the DNA microarray datasets obtained under various conditions and methods. In this study, we grouped homologous genes to perform a meta-analysis of multiple vascular endothelial cell and skeletal muscle datasets. According to the t-distributed stochastic neighbor embedding (t-SNE) analysis, the changes in the gene expression pattern in vascular endothelial cells formed specific clusters. We also identified candidate genes in endothelial cells that responded to gravity. Further, we exposed human umbilical vein endothelial cells (HUVEC) to simulated microgravity (SMG) using a clinostat and measured the expression levels of the candidate genes. Gene expression analysis using qRT-PCR revealed that the expression level of the prostaglandin (PG) transporter gene SLCO2A1 decreased in response to microgravity, consistent with the meta-analysis of microarray datasets. Furthermore, the direction of gravity affected the expression level of SLCO2A1, buttressing the finding that its expression was affected by gravity. These results suggest that a meta-analysis of DNA microarray datasets may help identify new target genes previously overlooked in individual microarray analyses.
en-copyright=
kn-copyright=

en-aut-name=LiangYin
en-aut-sei=Liang
en-aut-mei=Yin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangMengxue
en-aut-sei=Wang
en-aut-mei=Mengxue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LiuYun
en-aut-sei=Liu
en-aut-mei=Yun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangChen
en-aut-sei=Wang
en-aut-mei=Chen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=DNA microarrays
kn-keyword=DNA microarrays
en-keyword=meta-analysis
kn-keyword=meta-analysis
en-keyword=microgravity
kn-keyword=microgravity
en-keyword=human umbilical vein endothelial cells
kn-keyword=human umbilical vein endothelial cells
en-keyword=prostaglandin transporter
kn-keyword=prostaglandin transporter
en-keyword=clinostat
kn-keyword=clinostat
en-keyword=spaceflight-associated neuro-ocular syndrome
kn-keyword=spaceflight-associated neuro-ocular syndrome
END

start-ver=1.4
cd-journal=joma
no-vol=566
cd-vols=
no-issue=
article-no=
start-page=190
end-page=196
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=2021820
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Role of the TRPM4 channel in mitochondrial function, calcium release, and ROS generation in oxidative stress
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ischemic heart disease is one of the most common causes of death worldwide. Mitochondrial
dysfunction, excessive reactive oxygen species (ROS) generation, and calcium (Ca2?) overload are three key factors leading to myocardial death during ischemia-reperfusion (I/R) injury. Inhibition of TRPM4, a Ca2?-activated nonselective cation channel, protects the rat heart from I/R injury, but the specific mechanism underlying this effect is unclear. In this study, we investigated the mechanism of cardioprotection against I/R injury via TRPM4 using hydrogen peroxide (H2O2), a major contributor to oxidative stress, as an I/R injury model. We knocked out the TRPM4 gene in the rat cardiomyocyte cell line H9c2 using CRISPR/Cas9. Upon H2O2 treatment, intracellular Ca2? level and ROS production increased in wild type (WT) cells but not in TRPM4 knockout (TRPM4KO) cells. With this treatment, two indicators of mitochondrial function, mitochondrial membrane potential (DJm) and intracellular ATP levels, decreased inWT but not in TRPM4KO cells. Taken together, these findings suggest that blockade of the TRPM4 channel might protect the myocardium from oxidative stress by maintaining the mitochondrial membrane potential and intracellular ATP levels, possibly through preventing aberrant increases in intracellular Ca2? and ROS.
en-copyright=
kn-copyright=

en-aut-name=WangChen
en-aut-sei=Wang
en-aut-mei=Chen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ChenJian
en-aut-sei=Chen
en-aut-mei=Jian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangMengxue
en-aut-sei=Wang
en-aut-mei=Mengxue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=22
cd-vols=
no-issue=4
article-no=
start-page=1729
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210209
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Treatment of Oxidative Stress with Exosomes in Myocardial Ischemia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A thrombus in a coronary artery causes ischemia, which eventually leads to myocardial infarction (MI) if not removed. However, removal generates reactive oxygen species (ROS), which causes ischemia-reperfusion (I/R) injury that damages the tissue and exacerbates the resulting MI. The mechanism of I/R injury is currently extensively understood. However, supplementation of exogenous antioxidants is ineffective against oxidative stress (OS). Enhancing the ability of endogenous antioxidants may be a more effective way to treat OS, and exosomes may play a role as targeted carriers. Exosomes are nanosized vesicles wrapped in biofilms which contain various complex RNAs and proteins. They are important intermediate carriers of intercellular communication and material exchange. In recent years, diagnosis and treatment with exosomes in cardiovascular diseases have gained considerable attention. Herein, we review the new findings of exosomes in the regulation of OS in coronary heart disease, discuss the possibility of exosomes as carriers for the targeted regulation of endogenous ROS generation, and compare the advantages of exosome therapy with those of stem-cell therapy. Finally, we explore several miRNAs found in exosomes against OS.
en-copyright=
kn-copyright=

en-aut-name=LiuYun
en-aut-sei=Liu
en-aut-mei=Yun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangMengxue
en-aut-sei=Wang
en-aut-mei=Mengxue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LiangYin
en-aut-sei=Liang
en-aut-mei=Yin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangChen
en-aut-sei=Wang
en-aut-mei=Chen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=exosome
kn-keyword=exosome
en-keyword=oxidative stress
kn-keyword=oxidative stress
en-keyword=exosome therapy
kn-keyword=exosome therapy
en-keyword=myocardial infarction
kn-keyword=myocardial infarction
en-keyword=coronary heart disease
kn-keyword=coronary heart disease
en-keyword=reactive oxygen radicals
kn-keyword=reactive oxygen radicals
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=
article-no=
start-page=2
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210208
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Gravity sensing in plant and animal cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Gravity determines shape of body tissue and affects the functions of life, both in plants and animals. The cellular response to gravity is an active process of mechanotransduction. Although plants and animals share some common mechanisms of gravity sensing in spite of their distant phylogenetic origin, each species has its own mechanism to sense and respond to gravity. In this review, we discuss current understanding regarding the mechanisms of cellular gravity sensing in plants and animals. Understanding gravisensing also contributes to life on Earth, e.g., understanding osteoporosis and muscle atrophy. Furthermore, in the current age of Mars exploration, understanding cellular responses to gravity will form the foundation of living in space.
en-copyright=
kn-copyright=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakahashiHideyuki
en-aut-sei=Takahashi
en-aut-mei=Hideyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FuruichiTakuya
en-aut-sei=Furuichi
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ToyotaMasatsugu
en-aut-sei=Toyota
en-aut-mei=Masatsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=Furutani-SeikiMakoto
en-aut-sei=Furutani-Seiki
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KobayashiTakeshi
en-aut-sei=Kobayashi
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=Watanabe-TakanoHaruko
en-aut-sei=Watanabe-Takano
en-aut-mei=Haruko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ShinoharaMasahiro
en-aut-sei=Shinohara
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=Numaga-TomitaTakuro
en-aut-sei=Numaga-Tomita
en-aut-mei=Takuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=Sakaue-SawanoAsako
en-aut-sei=Sakaue-Sawano
en-aut-mei=Asako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MiyawakiAtsushi
en-aut-sei=Miyawaki
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=3
en-affil=Faculty of Human Life Sciences, Hagoromo University of International Studies
kn-affil=

affil-num=4
en-affil=Department of Biochemistry and Molecular Biology, Saitama University
kn-affil=

affil-num=5
en-affil=Department of Systems Biochemistry in Regeneration and Pathology, Graduate School of Medicine, Yamaguchi University
kn-affil=

affil-num=6
en-affil=Department of Integrative Physiology, Graduate School of Medicine, Nagoya University
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, National Cerebral and Cardiovascular Center Research Institute
kn-affil=

affil-num=8
en-affil=Department of Rehabilitation for the Movement Functions, Research Institute, National Rehabilitation Center for Persons with Disabilities
kn-affil=

affil-num=9
en-affil=Department of Molecular Pharmacology, Shinshu University School of Medicine
kn-affil=

affil-num=10
en-affil=Lab for Cell Function and Dynamics, CBS, RIKEN
kn-affil=

affil-num=11
en-affil=Lab for Cell Function and Dynamics, CBS, RIKEN
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=21
cd-vols=
no-issue=24
article-no=
start-page=9352
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20201208
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Inhibitory Role of Rab11b in Osteoclastogenesis through Triggering Lysosome-Induced Degradation of c-Fms and RANK Surface Receptors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Rab11b, abundantly enriched in endocytic recycling compartments, is required for the establishment of the machinery of vesicle trafficking. Yet, no report has so far characterized the biological function of Rab11b in osteoclastogenesis. Using in vitro model of osteoclasts differentiated from murine macrophages like RAW-D cells or bone marrow-derived macrophages, we elucidated that Rab11b served as an inhibitory regulator of osteoclast differentiation sequentially via (i) abolishing surface abundance of RANK and c-Fms receptors; and (ii) attenuating nuclear factor of activated T-cells c1 (NFATc-1) upstream signaling cascades, following RANKL stimulation. Rab11b was localized in early and late endosomes, Golgi complex, and endoplasmic reticulum; moreover, its overexpression enlarged early and late endosomes. Upon inhibition of lysosomal function by a specific blocker, chloroquine (CLQ), we comprehensively clarified a novel function of lysosomes on mediating proteolytic degradation of c-Fms and RANK surface receptors, drastically ameliorated by Rab11b overexpression in RAW-D cell-derived osteoclasts. These findings highlight the key role of Rab11b as an inhibitor of osteoclastogenesis by directing the transport of c-Fms and RANK surface receptors to lysosomes for degradation via the axis of early endosomes-late endosomes-lysosomes, thereby contributing towards the systemic equilibrium of the bone resorption phase.
en-copyright=
kn-copyright=

en-aut-name=TranManh Tien
en-aut-sei=Tran
en-aut-mei=Manh Tien
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkushaYuka
en-aut-sei=Okusha
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FengYunxia
en-aut-sei=Feng
en-aut-mei=Yunxia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MorimatsuMasatoshi
en-aut-sei=Morimatsu
en-aut-mei=Masatoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WeiPenggong
en-aut-sei=Wei
en-aut-mei=Penggong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SogawaChiharu
en-aut-sei=Sogawa
en-aut-mei=Chiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=EguchiTakanori
en-aut-sei=Eguchi
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KadowakiTomoko
en-aut-sei=Kadowaki
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SakaiEiko
en-aut-sei=Sakai
en-aut-mei=Eiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OkamuraHirohiko
en-aut-sei=Okamura
en-aut-mei=Hirohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TsukubaTakayuki
en-aut-sei=Tsukuba
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OkamotoKuniaki
en-aut-sei=Okamoto
en-aut-mei=Kuniaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Frontier Oral Science, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=9
en-affil=Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=10
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=13
en-affil=Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Rab11b
kn-keyword=Rab11b
en-keyword=c-Fms
kn-keyword=c-Fms
en-keyword=RANK
kn-keyword=RANK
en-keyword=NFATc-1
kn-keyword=NFATc-1
en-keyword=osteoclasts
kn-keyword=osteoclasts
en-keyword=vesicular transport
kn-keyword=vesicular transport
END

start-ver=1.4
cd-journal=joma
no-vol=132
cd-vols=
no-issue=2
article-no=
start-page=110
end-page=111
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200803
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 59th Annual Conference of Japanese Society for Medical and Biological Engineering
kn-title=第59回日本生体医工学会大会開催報告
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=成瀬恵治
kn-aut-sei=成瀬
kn-aut-mei=恵治
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=岡山大学大学院医歯薬学総合研究科　システム生理学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=159
article-no=
start-page=e61104
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200505
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Model of Ischemic Heart Disease and Video-Based Comparison of Cardiomyocyte Contraction Using hiPSC-Derived Cardiomyocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ischemic heart disease is a significant cause of death worldwide. It has therefore been the subject of a tremendous amount of research, often with small-animal models such as rodents. However, the physiology of the human heart differs significantly from that of the rodent heart, underscoring the need for clinically relevant models to study heart disease. Here, we present a protocol to model ischemic heart disease using cardiomyocytes differentiated from human induced pluripotent stem cells (hiPS-CMs) and to quantify the damage and functional impairment of the ischemic cardiomyocytes. Exposure to 2% oxygen without glucose and serum increases the percentage of injured cells, which is indicated by staining of the nucleus with propidium iodide, and decreases cellular viability. These conditions also decrease the contractility of hiPS-CMs as confirmed by displacement vector field analysis of microscopic video images. This protocol may furthermore provide a convenient method for personalized drug screening by facilitating the use of hiPS cells from individual patients. Therefore, this model of ischemic heart disease, based on iPS-CMs of human origin, can provide a useful platform for drug screening and further research on ischemic heart disease.
en-copyright=
kn-copyright=

en-aut-name=LiuYun
en-aut-sei=Liu
en-aut-mei=Yun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=LiangYin
en-aut-sei=Liang
en-aut-mei=Yin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangMengxue
en-aut-sei=Wang
en-aut-mei=Mengxue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangChen
en-aut-sei=Wang
en-aut-mei=Chen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=Wei Heng
en-aut-sei=Wei
en-aut-mei= Heng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Institute of Laboratory Animals, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Medicine
kn-keyword=Medicine
en-keyword=Issue 159
kn-keyword=Issue 159
en-keyword=Ischemic heart disease
kn-keyword=Ischemic heart disease
en-keyword= hypoxia, Myocardial infarction
kn-keyword= hypoxia, Myocardial infarction
en-keyword=Human induced pluripotent stem cells
kn-keyword=Human induced pluripotent stem cells
en-keyword=cellular differentiation
kn-keyword=cellular differentiation
en-keyword=Cardiomyocytes
kn-keyword=Cardiomyocytes
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=
article-no=
start-page=307
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200602
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=In vitroNeo-Genesis of Tendon/Ligament-Like Tissue by Combination of Mohawk and a Three-Dimensional Cyclic Mechanical Stretch Culture System
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Tendons and ligaments are pivotal connective tissues that tightly connect muscle and bone. In this study, we developed a novel approach to generate tendon/ligament-like tissues with a hierarchical structure, by introducing the tendon/ligament-specific transcription factor Mohawk (MKX) into the mesenchymal stem cell (MSC) line C3H10T1/2 cells, and by applying an improved three-dimensional (3D) cyclic mechanical stretch culture system. In our developed protocol, a combination of stableMkxexpression and cyclic mechanical stretch synergistically affects the structural tendon/ligament-like tissue generation and tendon related gene expression. In a histological analysis of these tendon/ligament-like tissues, an organized extracellular matrix (ECM), containing collagen type III and elastin, was observed. Moreover, we confirmed thatMkxexpression and cyclic mechanical stretch, induced the alignment of structural collagen fibril bundles that were deposited in a fibripositor-like manner during the generation of our tendon/ligament-like tissues. Our findings provide new insights for the tendon/ligament biomaterial fields.
en-copyright=
kn-copyright=

en-aut-name=KataokaKensuke
en-aut-sei=Kataoka
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KurimotoRyota
en-aut-sei=Kurimoto
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsutsumiHiroki
en-aut-sei=Tsutsumi
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ChibaTomoki
en-aut-sei=Chiba
en-aut-mei=Tomoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KatoTomomi
en-aut-sei=Kato
en-aut-mei=Tomomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShishidoKana
en-aut-sei=Shishido
en-aut-mei=Kana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KatoMariko
en-aut-sei=Kato
en-aut-mei=Mariko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ItoYoshiaki
en-aut-sei=Ito
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ChoYuichiro
en-aut-sei=Cho
en-aut-mei=Yuichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HoshiOsamu
en-aut-sei=Hoshi
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MimataAyako
en-aut-sei=Mimata
en-aut-mei=Ayako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SakamakiYuriko
en-aut-sei=Sakamaki
en-aut-mei=Yuriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=NakamichiRyo
en-aut-sei=Nakamichi
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=LotzMartin K.
en-aut-sei=Lotz
en-aut-mei=Martin K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=AsaharaHiroshi
en-aut-sei=Asahara
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Department of Systems BioMedicine, Tokyo Medical and Dental University
kn-affil=

affil-num=2
en-affil=Department of Systems BioMedicine, Tokyo Medical and Dental University
kn-affil=

affil-num=3
en-affil=Department of Systems BioMedicine, Tokyo Medical and Dental University
kn-affil=

affil-num=4
en-affil=Department of Systems BioMedicine, Tokyo Medical and Dental University
kn-affil=

affil-num=5
en-affil=Department of Systems BioMedicine, Tokyo Medical and Dental University
kn-affil=

affil-num=6
en-affil=Department of Systems BioMedicine, Tokyo Medical and Dental University
kn-affil=

affil-num=7
en-affil=Department of Systems BioMedicine, Tokyo Medical and Dental University
kn-affil=

affil-num=8
en-affil=Department of Systems BioMedicine, Tokyo Medical and Dental University
kn-affil=

affil-num=9
en-affil=Anatomy and Physiological Science, Tokyo Medical and Dental University
kn-affil=

affil-num=10
en-affil=Anatomy and Physiological Science, Tokyo Medical and Dental University
kn-affil=

affil-num=11
en-affil=Research Core, Tokyo Medical and Dental University
kn-affil=

affil-num=12
en-affil=Research Core, Tokyo Medical and Dental University
kn-affil=

affil-num=13
en-affil=Department of Systems BioMedicine, Tokyo Medical and Dental University
kn-affil=

affil-num=14
en-affil=Department of Molecular Medicine, The Scripps Research Institute
kn-affil=

affil-num=15
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=16
en-affil=Department of Systems BioMedicine, Tokyo Medical and Dental University
kn-affil=
en-keyword=Mohawk
kn-keyword=Mohawk
en-keyword=tendon
kn-keyword=tendon
en-keyword=ligament
kn-keyword=ligament
en-keyword=tissue engineering
kn-keyword=tissue engineering
en-keyword=mechanical-stress
kn-keyword=mechanical-stress
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=
article-no=
start-page=5754
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20191217
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Elimination of fukutin reveals cellular and molecular pathomechanisms in muscular dystrophy-associated heart failure
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Heart failure is the major cause of death for muscular dystrophy patients, however, the molecular pathomechanism remains unknown. Here, we show the detailed molecular pathogenesis of muscular dystrophy-associated cardiomyopathy in mice lacking the fukutin gene (Fktn), the causative gene for Fukuyama muscular dystrophy. Although cardiac Fktn elimination markedly reduced alpha-dystroglycan glycosylation and dystrophin-glycoprotein complex proteins in sarcolemma at all developmental stages, cardiac dysfunction was observed only in later adulthood, suggesting that membrane fragility is not the sole etiology of cardiac dysfunction. During young adulthood, Fktn-deficient mice were vulnerable to pathological hypertrophic stress with downregulation of Akt and the MEF2-histone deacetylase axis. Acute Fktn elimination caused severe cardiac dysfunction and accelerated mortality with myocyte contractile dysfunction and disordered Golgi-microtubule networks, which were ameliorated with colchicine treatment. These data reveal fukutin is crucial for maintaining myocyte physiology to prevent heart failure, and thus, the results may lead to strategies for therapeutic intervention.
en-copyright=
kn-copyright=

en-aut-name=UjiharaYoshihiro
en-aut-sei=Ujihara
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KanagawaMotoi
en-aut-sei=Kanagawa
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MohriSatoshi
en-aut-sei=Mohri
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakatsuSatomi
en-aut-sei=Takatsu
en-aut-mei=Satomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KobayashiKazuhiro
en-aut-sei=Kobayashi
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KatanosakaYuki
en-aut-sei=Katanosaka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Division of Neurology/Molecular Brain Science, Kobe University Graduate School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Division of Neurology/Molecular Brain Science, Kobe University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Division of Neurology/Molecular Brain Science, Kobe University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=520
cd-vols=
no-issue=3
article-no=
start-page=600
end-page=605
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20191210
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Development of a model of ischemic heart disease using cardiomyocytes differentiated from human induced pluripotent stem cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ischemic heart disease remains the largest cause of death worldwide. Accordingly, many researchers have sought curative options, often using laboratory animal models such as rodents. However, the physiology of the human heart differs significantly from that of the rodent heart. In this study, we developed a model of ischemic heart disease using cardiomyocytes differentiated from human induced pluripotent stem cells (hiPS-CMs). After optimizing the conditions of ischemia, including the concentration of oxygen and duration of application, we evaluated the consequent damage to hiPS-CMs. Notably, exposure to 2% oxygen, 0 mg/ml glucose, and 0% fetal bovine serum increased the percentage of nuclei stained with propidium iodide, an indicator of membrane damage, and decreased cellular viability. These conditions also decreased the contractility of hiPS-CMs. Furthermore, ischemic conditioning increased the mRNA expression of IL-8, consistent with observed conditions in the in vivo heart. Taken together, these findings suggest that our hiPS-CM-based model can provide a useful platform for human ischemic heart disease research.
en-copyright=
kn-copyright=

en-aut-name=WeiHeng
en-aut-sei=Wei
en-aut-mei=Heng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangChen
en-aut-sei=Wang
en-aut-mei=Chen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=GuoRui
en-aut-sei=Guo
en-aut-mei=Rui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Cardiomyocytes
kn-keyword=Cardiomyocytes
en-keyword=Human induced pluripotent stem cells
kn-keyword=Human induced pluripotent stem cells
en-keyword=Ischemic heart disease
kn-keyword=Ischemic heart disease
en-keyword=Myocardial infarction
kn-keyword=Myocardial infarction
END

start-ver=1.4
cd-journal=joma
no-vol=383
cd-vols=
no-issue=2
article-no=
start-page=111556
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20191015
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mechanical strain attenuates cytokine-induced ADAMTS9 expression via transient receptor potential vanilloid type 1
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= The synovial fluids of patients with osteoarthritis (OA) contain elevated levels of inflammatory cytokines, which induce the expression of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) and of the matrix metalloproteinase (MMP) in chondrocytes. Mechanical strain has varying effects on organisms depending on the strength, cycle, and duration of the stressor; however, it is unclear under inflammatory stimulation how mechanical strain act on. Here, we show that mechanical strain attenuates inflammatory cytokine-induced expression of matrix-degrading enzymes. Cyclic tensile strain (CTS), as a mechanical stressor, attenuated interleukin (IL)-1β and tumor necrosis factor (TNF)-α-induced mRNA expression of ADAMTS4, ADAMTS9, and MMP-13 in normal chondrocytes (NHAC-kn) and in a chondrocytic cell line (OUMS-27). This effect was abolished by treating cells with mechano-gated channel inhibitors, such as gadolinium, transient receptor potential (TRP) family inhibitor, ruthenium red, and with pharmacological and small interfering RNA-mediated TRPV1 inhibition. Furthermore, nuclear factor κB (NF-κB) translocation from the cytoplasm to the nucleus resulting from cytokine stimulation was also abolished by CTS. These findings suggest that mechanosensors such as the TRPV protein are potential therapeutic targets in treating OA.
en-copyright=
kn-copyright=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShinaokaAkira
en-aut-sei=Shinaoka
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Kumagishi-ShinaokaKanae
en-aut-sei=Kumagishi-Shinaoka
en-aut-mei=Kanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AsanoKeiichi
en-aut-sei=Asano
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HatipogluOmer Faruk
en-aut-sei=Hatipoglu
en-aut-mei=Omer Faruk
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=InagakiJunko
en-aut-sei=Inagaki
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NishidaKeiichiro
en-aut-sei=Nishida
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HirohataSatoshi
en-aut-sei=Hirohata
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Orthopaedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=
article-no=
start-page=3932
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140529
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=TRPV2 is critical for the maintenance of cardiac structure and function in mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The heart has a dynamic compensatory mechanism for haemodynamic stress. However, the molecular details of how mechanical forces are transduced in the heart are unclear. Here we show that the transient receptor potential, vanilloid family type 2 (TRPV2) cation channel is critical for the maintenance of cardiac structure and function. Within 4 days of eliminating TRPV2 from hearts of the adult mice, cardiac function declines severely, with disorganization of the intercalated discs that support mechanical coupling with neighbouring myocytes and myocardial conduction defects. After 9 days, cell shortening and Ca2+ handling by single myocytes are impaired in TRPV2-deficient hearts. TRPV2-deficient neonatal cardiomyocytes form no intercalated discs and show no extracellular Ca2+-dependent intracellular Ca2+ increase and insulin-like growth factor (IGF-1) secretion in response to stretch stimulation. We further demonstrate that IGF-1 receptor/PI3K/Akt pathway signalling is significantly downregulated in TRPV2-deficient hearts, and that IGF-1 administration partially prevents chamber dilation and impairment in cardiac pump function in these hearts. Our results improve our understanding of the molecular processes underlying the maintenance of cardiac structure and function.
en-copyright=
kn-copyright=

en-aut-name=KatanosakaYuki
en-aut-sei=Katanosaka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IwasakiKeiichiro
en-aut-sei=Iwasaki
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UjiharaYoshihiro
en-aut-sei=Ujihara
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakatsuSatomi
en-aut-sei=Takatsu
en-aut-mei=Satomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NishitsujiKoki
en-aut-sei=Nishitsuji
en-aut-mei=Koki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KanagawaMotoi
en-aut-sei=Kanagawa
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SudoAtsushi
en-aut-sei=Sudo
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KatanosakaKimiaki
en-aut-sei=Katanosaka
en-aut-mei=Kimiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MohriSatoshi
en-aut-sei=Mohri
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=2
en-affil=
kn-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=3
en-affil=
kn-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=4
en-affil=
kn-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=5
en-affil=
kn-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=6
en-affil=
kn-affil=Division of Neurology/Molecular Brain Science, Kobe University Graduate School of Medicine

affil-num=7
en-affil=
kn-affil=Division of Neurology/Molecular Brain Science, Kobe University Graduate School of Medicine

affil-num=8
en-affil=
kn-affil=Division of Neurology/Molecular Brain Science, Kobe University Graduate School of Medicine

affil-num=9
en-affil=
kn-affil=Department of Neuroscience II, Research Institute of Environmental Medicine, Nagoya University

affil-num=10
en-affil=
kn-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=11
en-affil=
kn-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=7
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140722
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Directed Differentiation of Patient-Specific Induced Pluripotent Stem Cells Identifies the Transcriptional Repression and Epigenetic Modification of NKX2-5, HAND1, and NOTCH1 in Hypoplastic Left Heart Syndrome
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The genetic basis of hypoplastic left heart syndrome (HLHS) remains unknown, and the lack of animal models to reconstitute the cardiac maldevelopment has hampered the study of this disease. This study investigated the altered control of transcriptional and epigenetic programs that may affect the development of HLHS by using disease-specific induced pluripotent stem (iPS) cells. Cardiac progenitor cells (CPCs) were isolated from patients with congenital heart diseases to generate patient-specific iPS cells. Comparative gene expression analysis of HLHS- and biventricle (BV) heart-derived iPS cells was performed to dissect the complex genetic circuits that may promote the disease phenotype. Both HLHS- and BV heart-derived CPCs were reprogrammed to generate disease-specific iPS cells, which showed characteristic human embryonic stem cell signatures, expressed pluripotency markers, and could give rise to cardiomyocytes. However, HLHS-iPS cells exhibited lower cardiomyogenic differentiation potential than BV-iPS cells. Quantitative gene expression analysis demonstrated that HLHS-derived iPS cells showed transcriptional repression of NKX2-5, reduced levels of TBX2 and NOTCH/HEY signaling, and inhibited HAND1/2 transcripts compared with control cells. Although both HLHS-derived CPCs and iPS cells showed reduced SRE and TNNT2 transcriptional activation compared with BV-derived cells, co-transfection of NKX2-5, HAND1, and NOTCH1 into HLHS-derived cells resulted in synergistic restoration of these promoters activation. Notably, gain- and loss-of-function studies revealed that NKX2-5 had a predominant impact on NPPA transcriptional activation. Moreover, differentiated HLHS-derived iPS cells showed reduced H3K4 dimethylation as well as histone H3 acetylation but increased H3K27 trimethylation to inhibit transcriptional activation on the NKX2-5 promoter. These findings suggest that patient-specific iPS cells may provide molecular insights into complex transcriptional and epigenetic mechanisms, at least in part, through combinatorial expression of NKX2-5, HAND1, and NOTCH1 that coordinately contribute to cardiac malformations in HLHS.
en-copyright=
kn-copyright=

en-aut-name=KobayashiJunko
en-aut-sei=Kobayashi
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TaruiSuguru
en-aut-sei=Tarui
en-aut-mei=Suguru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HirataMasataka
en-aut-sei=Hirata
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NagaiYusuke
en-aut-sei=Nagai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KasaharaShingo
en-aut-sei=Kasahara
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SanoShunji
en-aut-sei=Sano
en-aut-mei=Shunji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OhHidemasa
en-aut-sei=Oh
en-aut-mei=Hidemasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Surg

affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Med

affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Surg

affil-num=4
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Surg

affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Physiol

affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Surg

affil-num=7
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Physiol

affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Med

affil-num=9
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Surg

affil-num=10
en-affil=
kn-affil=Okayama Univ Hosp, Dept Regenerat Med, Ctr Innovat Clin Med
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=7
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140721
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Neutral Self-Assembling Peptide Hydrogel SPG-178 as a Topical Hemostatic Agent
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Conventional self-assembling peptide hydrogels are effective as topical hemostatic agents. However, there is a possibility to harm living tissues due to their low pH. The aim of the present study was to demonstrate the efficacy of SPG-178, a neutral self-assembling peptide hydrogel, as a topical hemostatic agent. First, we measured the bleeding duration of incisions made on rat livers after application of SPG-178 (1.0% w/v), SPG-178 (1.5% w/v), RADA16 (1.0% w/v), and saline (n = 12/group). Second, we observed the bleeding surfaces by transmission electron microscopy immediately after hemostasis. Third, we measured the elastic and viscous responses (G′ and G″, respectively) of the hydrogels using a rheometer. Our results showed that bleeding duration was significantly shorter in the SPG-178 group than in the RADA16 group and that there were no significant differences in transmission electron microscopy findings between the groups. The greater the G′ value of a hydrogel, the shorter was the bleeding duration. We concluded that SPG-178 is more effective and has several advantages: it is non-biological, transparent, nonadherent, and neutral and can be sterilized by autoclaving.
en-copyright=
kn-copyright=

en-aut-name=KomatsuSeiji
en-aut-sei=Komatsu
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NagaiYusuke
en-aut-sei=Nagai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KimataYoshihiro
en-aut-sei=Kimata
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Plastic and Reconstructive Surgery, Okayama Saiseikai General Hospital

affil-num=2
en-affil=
kn-affil=Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Plastic and Reconstructive Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
END

start-ver=1.4
cd-journal=joma
no-vol=126
cd-vols=
no-issue=1
article-no=
start-page=7
end-page=10
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The mechanical stimulation of cells in 3D culture within a self-assembling peptide hydrogel
kn-title=自己集合性ペプチドハイドロゲル内で三次元培養された細胞への機械刺激
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NagaiYusuke
en-aut-sei=Nagai
en-aut-mei=Yusuke
kn-aut-name=永井祐介
kn-aut-sei=永井
kn-aut-mei=祐介
aut-affil-num=1
ORCID=

en-aut-name=YokoiHidenori
en-aut-sei=Yokoi
en-aut-mei=Hidenori
kn-aut-name=横井秀典
kn-aut-sei=横井
kn-aut-mei=秀典
aut-affil-num=2
ORCID=

en-aut-name=KaiharaKeiko
en-aut-sei=Kaihara
en-aut-mei=Keiko
kn-aut-name=貝原恵子
kn-aut-sei=貝原
kn-aut-mei=恵子
aut-affil-num=3
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=成瀬恵治
kn-aut-sei=成瀬
kn-aut-mei=恵治
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　システム生理学

affil-num=2
en-affil=
kn-affil=株式会社メニコン

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　システム生理学

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　システム生理学
en-keyword=機械刺激
kn-keyword=機械刺激
en-keyword=メカノバイオロジー
kn-keyword=メカノバイオロジー
en-keyword=自己集合性ペプチド
kn-keyword=自己集合性ペプチド
en-keyword=３次元培養
kn-keyword=３次元培養
en-keyword=スキャフォールド
kn-keyword=スキャフォールド
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=243
end-page=262
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120912
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Use of Silicone Elastomer-Based Microfluidic Devices and Systems in Reproductive Technologies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MatsuuraKoji
en-aut-sei=Matsuura
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=
kn-affil=Research Core for Interdisciplinary Sciences, Okayama University

affil-num=2
en-affil=
kn-affil=Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=1
article-no=
start-page=109
end-page=115
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Screening of sperm velocity by fluid mechanical characteristics of a cyclo-olefin polymer microfluidic sperm-sorting device
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The microfluidic sperm-sorting (MFSS) device is a promising advancement for assisted reproductive technology. Previously, poly(dimethylsiloxiane) and quartz MFSS devices were developed and used for intracytoplasmic sperm injection. However, these disposable devices were not clinically suitable for assisted reproduction, so a cyclo-olefin polymer MFSS (COP-MFSS) device was developed. By micromachining, two microfluidic channels with different heights and widths (chip A: 0.3 x 0.5 mm; chip B: 0.1 x 0.6 mm) were prepared. Sorted sperm concentrations were similar in both microfluidic channels. Linear-velocity distribution using the microfluidic channel of chip B was higher than that of chip A. Using confocal fluorescence microscopy, it was found that the highest number of motile spermatozoa swam across the laminar flow at the bottom of the microfluidic channel. The time required to swim across the laminar flow was longer at the bottom and top of the microfluidic channels than in the middle because of the low fluid velocity. These results experimentally demonstrated that the width of microfluidic channels should be increased in the region of laminar flow from the semen inlet to the outlet for unsorted spermatozoa to selectively recover spermatozoa with high linear velocity.
en-copyright=
kn-copyright=

en-aut-name=MatsuuraKoji
en-aut-sei=Matsuura
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakenamiMami
en-aut-sei=Takenami
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KurodaYuka
en-aut-sei=Kuroda
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HyakutakeToru
en-aut-sei=Hyakutake
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YanaseShinichiro
en-aut-sei=Yanase
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Research Core for Interdisciplinary Sciences, Okayama University

affil-num=2
en-affil=
kn-affil=Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=3
en-affil=
kn-affil=Research Core for Interdisciplinary Sciences, Okayama University

affil-num=4
en-affil=
kn-affil=Faculty of Engineering, Yokohama National University

affil-num=5
en-affil=
kn-affil=Graduate School of Natural Science and Technology, Okayama University

affil-num=6
en-affil=
kn-affil=Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
en-keyword=laminar flow
kn-keyword=laminar flow
en-keyword=linear velocity
kn-keyword=linear velocity
en-keyword=microfluidic sperm sorting
kn-keyword=microfluidic sperm sorting
en-keyword=motility
kn-keyword=motility
END

start-ver=1.4
cd-journal=joma
no-vol=94
cd-vols=
no-issue=3
article-no=
start-page=1135
end-page=1137
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=201008
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Blastocyst quality scoring based on morphologic grading correlates with cell number
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Blastocyst quality score (BQS), first reported by Rehman et al., is a numerical blastocyst-morphology grading system based on the criteria established by Gardner and Schoolcraft. We demonstrate a positive correlation between the calculated BQS score and cell number by staining thawed human embryos and suggest that BQS can be applied to evaluate culture systems clinically.
en-copyright=
kn-copyright=

en-aut-name=MatsuuraKoji
en-aut-sei=Matsuura
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HayashiNobuyoshi
en-aut-sei=Hayashi
en-aut-mei=Nobuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakiueChisato
en-aut-sei=Takiue
en-aut-mei=Chisato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HirataRei
en-aut-sei=Hirata
en-aut-mei=Rei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HabaraToshihiro
en-aut-sei=Habara
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=2
en-affil=
kn-affil=Okayama Couples Clinic

affil-num=3
en-affil=
kn-affil=Okayama Couples Clinic

affil-num=4
en-affil=
kn-affil=Okayama Couples Clinic

affil-num=5
en-affil=
kn-affil=Okayama Couples Clinic

affil-num=6
en-affil=
kn-affil=Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
END

start-ver=1.4
cd-journal=joma
no-vol=74
cd-vols=
no-issue=5
article-no=
start-page=863
end-page=870
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100915
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Application of a microfluidic sperm sorter to the in-vitro fertilization of porcine oocytes reduced the incidence of polyspermic penetration
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The objective of this study was to use a microfluidic sperm sorter (MFSS), designed to isolate motile human spermatozoa with laminar flows (no centrifugation), for porcine IVF. Boar spermatozoa were diluted at 1 x 10(8) with a diluent containing 20% seminal fluid and flowed with modified TCM-199 (mM199, with 5 mM caffeine) to introduce motile sperm into the exit chamber for IVF. In Experiment 1, after flowing for 5 min, sperm concentration varied significantly among specific sites within the MFSS collecting chamber (range, 0.8 +/- 0.5 x 10(4) to 575.0 +/- 56.3 x 10(4) cells/mL; mean +/- SEM). In Experiment 2, when porcine IVM oocytes were placed at three locations in the MFSS exit chamber (where only motile spermatozoa accumulated) and subsequently cultured in caffeine-free mM199 for 8 h, sperm penetration rate was not significantly different among places (86.1 +/- 10.5 to 100%), but the monospermic penetration rate was lower (P < 0.05) in oocytes 3.5 mm from the exit position (12.5 +/- 4.8%) than those at 7.5 mm (53.1 +/- 6.0%) or further (41.9 +/- 2.8%) from the exit. In Experiment 3, the normal fertilization index (ratio of monospermic oocytes to number of oocytes examined) 8 h after insemination was higher (P < 0.05) in the MFSS-IVF system (0.375 +/- 0.040) than both standard IVF and transient IVF (0.222 +/- 0.028 and 0.189 +/- 0.027, respectively, with co-culture for 8 h and for 5 min). Developmental competence of fertilized oocytes (blastocyst formation) was higher (P < 0.05) in the MFSS-IVF system (40.9 +/- 2.3%) than in either standard or transient IVF (22.6 +/- 1.4 and 33.7 +/- 3.5%). In conclusion, brief co-culture of porcine oocytes with spermatozoa gradually accumulated in the MFSS chamber improved the efficiency of producing monospermic fertilized embryos and blastocysts. Furthermore, efficiencies were significantly affected by oocyte location within the chamber.
en-copyright=
kn-copyright=

en-aut-name=SanoHikaru
en-aut-sei=Sano
en-aut-mei=Hikaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuuraKoji
en-aut-sei=Matsuura
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FunahashiHiroaki
en-aut-sei=Funahashi
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Animal Science, Graduate school of Natural Science and Technology, Okayama University

affil-num=2
en-affil=
kn-affil=Cardiovascular Physiology, Graduate school of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=3
en-affil=
kn-affil=Cardiovascular Physiology, Graduate school of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=4
en-affil=
kn-affil=Department of Animal Science, Graduate school of Natural Science and Technology, Okayama University
en-keyword=Oocytes
kn-keyword=Oocytes
en-keyword=Polyspermy
kn-keyword=Polyspermy
en-keyword=IVF
kn-keyword=IVF
en-keyword=Sperm sorter
kn-keyword=Sperm sorter
en-keyword=Pig
kn-keyword=Pig
END

start-ver=1.4
cd-journal=joma
no-vol=56
cd-vols=
no-issue=5
article-no=
start-page=552
end-page=557
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=201010
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=In-vitro Culture with a Tilting Device in Chemically Defined Media During Meiotic Maturation and Early Development Improves the Quality of Blastocysts Derived from In-vitro Matured and Fertilized Porcine Oocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Under physiological conditions, mammalian oocytes and embryos appear to be stimulated not only chemically but also mechanically, such as by compression, shear stress and/or friction force in the follicle and female reproductive tract. The present study was undertaken to examine the effects of kinetic culture with a tilting device in chemically defined media during in vitro maturation (IVM) of porcine oocytes and in vitro culture (IVC) following in vitro fertilization (IVF) on the early developmental competence and quality of blastocysts. After culture in a chemically defined IVM medium, modified porcine oocyte medium (mPOM) containing gonadotropins and dibutyryl cAMP for 20 h, the mean diameter of the cumulus-oocyte complexes (COCs) was larger in the tilting culture than in the static controls, whereas the diameter of the oocytes did not differ. When culture of the COCs was continued additionally in a fresh medium without gonadotropins and dibutyryl cAMP for 24 h, the incidences of oocytes completing GVBD and developing to the metaphase-II stage did not differ between the tilting and static culture systems. Furthermore, the sperm penetration after IVF and developmental competence of the oocytes to the blastocyst stage were not different between the tilting and static systems during IVM and IVC. However, tilting culture during both IVM and IVC had a significant positive effect on the number of cells per blastocyst (P<0.05). These observations indicate that tilting culture during IVM and IVC in chemically defined media improves the quality of blastocyst, as determined by the number of cells per blastocyst, without any effects on penetrability and developmental competence.
en-copyright=
kn-copyright=

en-aut-name=KoikeTakayuki
en-aut-sei=Koike
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuuraKoji
en-aut-sei=Matsuura
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FunahashiHiroaki
en-aut-sei=Funahashi
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Animal Science, Graduate School of Natural Science and Technology, Okayama University

affil-num=2
en-affil=
kn-affil=Research Core for Interdisciplinary Sciences, Okayama University

affil-num=3
en-affil=
kn-affil=Department of Cardiovascular Physiology, Graduate school of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=4
en-affil=
kn-affil=Department of Animal Science, Graduate School of Natural Science and Technology, Okayama University
en-keyword=Inclining device
kn-keyword=Inclining device
en-keyword=In vitro culture
kn-keyword=In vitro culture
en-keyword=In vitro fertilization
kn-keyword=In vitro fertilization
en-keyword=Oocytes
kn-keyword=Oocytes
en-keyword=Pig
kn-keyword=Pig
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=1
article-no=
start-page=25
end-page=33
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=200902
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Application of a numerical simulation to improve the separation efficiency of a sperm sorter
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This paper describes a study in which numerical simulations were applied to improve the separation efficiency of a microfluidic-based sperm sorter. Initially, the motion of 31 sperm were modeled as a sinusoidal wave. The modeled sperm were expected to move while vibrating in the fluid within the microchannel. In this analysis, the number of sperm extracted at the outlet channel and the rate of movement of the highly motile sperm were obtained for a wide range of flow velocities within the microchannel. By varying the channel height, and the width and the position of the sperm-inlet channel, we confirmed that the separation efficiency was highly dependent on the fluid velocity within the channel. These results will be valuable for improving the device configuration, and might help to realize further improvements in efficiency in the future.
en-copyright=
kn-copyright=

en-aut-name=HyakutakeToru
en-aut-sei=Hyakutake
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HashimotoYuki
en-aut-sei=Hashimoto
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YanaseShinichiro
en-aut-sei=Yanase
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsuuraKoji
en-aut-sei=Matsuura
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Graduate School of Natural Science and Technology, Okayama University

affil-num=2
en-affil=
kn-affil=Graduate School of Natural Science and Technology, Okayama University

affil-num=3
en-affil=
kn-affil=Graduate School of Natural Science and Technology, Okayama University

affil-num=4
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=5
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
en-keyword=Human reproduction
kn-keyword=Human reproduction
en-keyword=Microfluid
kn-keyword=Microfluid
en-keyword=Numerical simulation
kn-keyword=Numerical simulation
en-keyword=Separation efficiency
kn-keyword=Separation efficiency
en-keyword=Sperm sorter
kn-keyword=Sperm sorter
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=22
article-no=
start-page=3306
end-page=3309
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=2009
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Fabricating small-scale, curved, polymeric structures with convex and concave menisci through interfacial free energy equilibrium
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Polymeric curved structures are widely used in imaging systems including optical fibers and microfluidic channels. Here, we demonstrate that small-scale, poly(dimethylsiloxane) (PDMS)-based, curved structures can be fabricated through controlling interfacial free energy equilibrium. Resultant structures have a smooth, symmetric, curved surface, and may be convex or concave in form based on surface tension balance. Their curvatures are controlled by surface characteristics (i.e., hydrophobicity and hydrophilicity) of the molds and semi-liquid PDMS. In addition, these structures are shown to be biocompatible for cell culture. Our system provides a simple, efficient and economical method for generating integrateable optical components without costly fabrication facilities.
en-copyright=
kn-copyright=

en-aut-name=ChengChao-Min
en-aut-sei=Cheng
en-aut-mei=Chao-Min
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuuraKoji
en-aut-sei=Matsuura
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangI-Jan
en-aut-sei=Wang
en-aut-mei=I-Jan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KurodaYuka
en-aut-sei=Kuroda
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=LeDucPhilip R.
en-aut-sei=LeDuc
en-aut-mei=Philip R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Departments of Mechanical and Biomedical Engineering and Biological Sciences, Carnegie Mellon University

affil-num=2
en-affil=
kn-affil=Research Core for Interdisciplinary Sciences, Okayama University

affil-num=3
en-affil=
kn-affil=Departments of Mechanical and Biomedical Engineering and Biological Sciences, Carnegie Mellon University

affil-num=4
en-affil=
kn-affil=Research Core for Interdisciplinary Sciences, Okayama University

affil-num=5
en-affil=
kn-affil=Departments of Mechanical and Biomedical Engineering and Biological Sciences, Carnegie Mellon University

affil-num=6
en-affil=
kn-affil=Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
END

start-ver=1.4
cd-journal=joma
no-vol=20
cd-vols=
no-issue=3
article-no=
start-page=358
end-page=364
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=201003
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Improved development of mouse and human embryos using a tilting embryo culture system
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mammalian embryos experience not only hormonal but also mechanical stimuli, such as shear stress, compression and friction force in the Fallopian tube before nidation. In order to apply mechanical stimuli to embryos in a conventional IVF culture system, the tilting embryo culture system (TECS) was developed. The observed embryo images from the TECS suggest that the velocities and shear stresses of TECS embryos are similar to those experienced in the oviduct. Use of TECS enhanced the development rate to the blastocyst stage and significantly increased the cell number of mouse blastocysts (P < 0.05). Although not statistically significant, human thawed embryos showed slight improvement in development to the blastocyst stage following culture in TECS compared with static controls. Rates of blastocyst formation following culture in TECS were significantly improved in low-quality embryos and those embryos cultured under suboptimal conditions (P < 0.05). The TECS is proposed as a promising approach to improve embryo development and blastocyst formation by exposing embryos to mechanical stimuli similar to those in the Fallopian tube.
en-copyright=
kn-copyright=

en-aut-name=MatsuuraKoji
en-aut-sei=Matsuura
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HayashiNobuyoshi
en-aut-sei=Hayashi
en-aut-mei=Nobuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KurodaYuka
en-aut-sei=Kuroda
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakiueChisato
en-aut-sei=Takiue
en-aut-mei=Chisato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HirataRei
en-aut-sei=Hirata
en-aut-mei=Rei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakenamiMami
en-aut-sei=Takenami
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AoiYoko
en-aut-sei=Aoi
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YoshiokaNanako
en-aut-sei=Yoshioka
en-aut-mei=Nanako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HabaraToshihiro
en-aut-sei=Habara
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MukaidaTetsunori
en-aut-sei=Mukaida
en-aut-mei=Tetsunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=
kn-affil=Research Core for Interdisciplinary Sciences, Okayama University

affil-num=2
en-affil=
kn-affil=Okayama Couples Clinic

affil-num=3
en-affil=
kn-affil=Research Core for Interdisciplinary Sciences, Okayama University

affil-num=4
en-affil=
kn-affil=Okayama Couples Clinic

affil-num=5
en-affil=
kn-affil=Okayama Couples Clinic

affil-num=6
en-affil=
kn-affil=Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=7
en-affil=
kn-affil=Okayama Couples Clinic

affil-num=8
en-affil=
kn-affil=Okayama Couples Clinic

affil-num=9
en-affil=
kn-affil=Okayama Couples Clinic

affil-num=10
en-affil=
kn-affil=Hiroshima HART Clinic

affil-num=11
en-affil=
kn-affil=Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
en-keyword=blastocyst
kn-keyword=blastocyst
en-keyword=embryo development
kn-keyword=embryo development
en-keyword=mechanical stimuli
kn-keyword=mechanical stimuli
en-keyword=shear stress
kn-keyword=shear stress
en-keyword=tilting embryo culture system
kn-keyword=tilting embryo culture system
END

start-ver=1.4
cd-journal=joma
no-vol=42
cd-vols=
no-issue=13
article-no=
start-page=2097
end-page=2103
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=20090918
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mechanical stretch stimulates integrin αVβ3-mediated collagen expression in human anterior cruciate ligament cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Biomechanical stimuli have fundamental roles in the maintenance and remodeling of ligaments including collagen gene expressions. Mechanical stretching signals are mainly transduced by cell adhesion molecules such as integrins. However, the relationships between stress-induced collagen expressions and integrin-mediated cellular behaviors are still unclear in anterior cruciate ligament cells. Here, we focused on the stretch-related responses of different cells derived from the ligament-to-bone interface and midsubstance regions of human anterior cruciate ligaments. Chondroblastic interface cells easily lost their potential to produce collagen genes in non-stretched conditions, rather than fibroblastic midsubstance cells. Uni-axial mechanical stretches increased the type I collagen gene expression of interface and midsubstance cells up to 14- and 6-fold levels of each non-stretched control, respectively. Mechanical stretches also activated the stress fiber formation by shifting the distribution of integrin αVβ3 to the peripheral edges in both interface and midsubstance cells. In addition, integrin αVβ3 colocalized with phosphorylated focal adhesion kinase in stretched cells. Functional blocking analyses using anti-integrin antibodies revealed that the stretch-activated collagen gene expressions on fibronectin were dependent on integrin αVβ3-mediated cellular adhesions in the interface and midsubstance cells. These findings suggest that the integrin αVβ3-mediated stretch signal transduction might have a key role to stimulate collagen gene expression in human anterior cruciate ligament, especially in the ligament-to-bone interface.
en-copyright=
kn-copyright=

en-aut-name=TetsunagaTomonori
en-aut-sei=Tetsunaga
en-aut-mei=Tomonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FurumatsuTakayuki
en-aut-sei=Furumatsu
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AbeNobuhiro
en-aut-sei=Abe
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NishidaKeiichiro
en-aut-sei=Nishida
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OzakiToshifumi
en-aut-sei=Ozaki
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Cardiovascular Physiology, Biophysiological Sciences, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Cardiovascular Physiology, Biophysiological Sciences, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
en-keyword=Anterior cruciateligament
kn-keyword=Anterior cruciateligament
en-keyword=Collagen
kn-keyword=Collagen
en-keyword=Integrin αVβ3
kn-keyword=Integrin αVβ3
en-keyword=Interface
kn-keyword=Interface
en-keyword=Mechanical stretch
kn-keyword=Mechanical stretch
END

start-ver=1.4
cd-journal=joma
no-vol=118
cd-vols=
no-issue=1
article-no=
start-page=23
end-page=31
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=20060501
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=メカノバイオロジー―基礎から臨床まで―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=成瀬恵治
kn-aut-sei=成瀬
kn-aut-mei=恵治
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　システム循環生理学
en-keyword=メカノトランスダクション
kn-keyword=メカノトランスダクション
en-keyword=ソフトリソグラフィー
kn-keyword=ソフトリソグラフィー
en-keyword=再生医療
kn-keyword=再生医療
en-keyword=不妊治療
kn-keyword=不妊治療
END