start-ver=1.4
cd-journal=joma
no-vol=87
cd-vols=
no-issue=11
article-no=
start-page=1323
end-page=1331
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230808
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The effect of exogenous dihydroxyacetone and methylglyoxal on growth, anthocyanin accumulation, and the glyoxalase system in Arabidopsis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Dihydroxyacetone (DHA) occurs in wide-ranging organisms, including plants, and can undergo spontaneous conversion to methylglyoxal (MG). While the toxicity of MG to plants is well-known, the toxicity of DHA to plants remains to be elucidated. We investigated the effects of DHA and MG on Arabidopsis. Exogenous DHA at up to 10 mM did not affect the radicle emergence, the expansion of green cotyledons, the seedling growth, or the activity of glyoxalase II, while DHA at 10 mM inhibited the root elongation and increased the activity of glyoxalase I. Exogenous MG at 1.0 mM inhibited these physiological responses and increased both activities. Dihydroxyacetone at 10 mM increased the MG content in the roots. These results indicate that DHA is not so toxic as MG in Arabidopsis seeds and seedlings and suggest that the toxic effect of DHA at high concentrations is attributed to MG accumulation by the conversion to MG.
en-copyright=
kn-copyright=
en-aut-name=ZhaoMaoxiang
en-aut-sei=Zhao
en-aut-mei=Maoxiang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=NakamuraToshiyuki
en-aut-sei=Nakamura
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=MunemasaShintaro
en-aut-sei=Munemasa
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=MoriIzumi C
en-aut-sei=Mori
en-aut-mei=Izumi C
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=3
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=5
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
affil-num=6
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=dihydroxyacetone
kn-keyword=dihydroxyacetone
en-keyword=methylglyoxal
kn-keyword=methylglyoxal
en-keyword=growth
kn-keyword=growth
en-keyword=anthocyanin
kn-keyword=anthocyanin
en-keyword=glyoxalase system
kn-keyword=glyoxalase system
END
start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=1
article-no=
start-page=e0296408
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240105
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Aromatic oil from lavender as an atopic dermatitis suppressant
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In atopic dermatitis (AD), nerves are abnormally stretched near the surface of the skin, making it sensitive to itching. Expression of neurotrophic factor Artemin (ARTN) involved in such nerve stretching is induced by the xenobiotic response (XRE) to air pollutants and UV radiation products. Therefore, AD can be monitored by the XRE response. Previously, we established a human keratinocyte cell line stably expressing a NanoLuc reporter gene downstream of XRE. We found that 6-formylindolo[3,2-b]carbazole (FICZ), a tryptophan metabolite and known inducer of the XRE, increased reporter and Artemin mRNA expression, indicating that FICZ-treated cells could be a model for AD. Lavender essential oil has been used in folk medicine to treat AD, but the scientific basis for its use is unclear. In the present study, we investigated the efficacy of lavender essential oil and its major components, linalyl acetate and linalool, to suppress AD and sensitize skin using the established AD model cell line, and keratinocyte and dendritic cell activation assays. Our results indicated that lavender essential oil from L. angustifolia and linalyl acetate exerted a strong AD inhibitory effect and almost no skin sensitization. Our model is useful in that it can circumvent the practice of using animal studies to evaluate AD medicines.
en-copyright=
kn-copyright=
en-aut-name=SatoHaruna
en-aut-sei=Sato
en-aut-mei=Haruna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=KatoKosuke
en-aut-sei=Kato
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=TsujinoYoshio
en-aut-sei=Tsujino
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=2
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=5
en-affil=Graduate School of Science, Technology, and Innovation, Kobe University
kn-affil=
affil-num=6
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
END
start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=1
article-no=
start-page=822
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230103
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cycloartenyl Ferulate Is the Predominant Compound in Brown Rice Conferring Cytoprotective Potential against Oxidative Stress-Induced Cytotoxicity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Since brown rice extract is a rich source of biologically active compounds, the present study is aimed to quantify the major compounds in brown rice and to compare their cytoprotective potential against oxidative stress. The content of the main hydrophobic compounds in brown rice followed the order of cycloartenyl ferulate (CAF) (89.00 +/- 8.07 nmol/g) >> alpha-tocopherol (alpha T) (19.73 +/- 2.28 nmol/g) > gamma-tocotrienol (gamma T3) (18.24 +/- 1.41 nmol/g) > alpha-tocotrienol (alpha T3) (16.02 +/- 1.29 nmol/g) > gamma-tocopherol (gamma T) (3.81 +/- 0.40 nmol/g). However, the percent contribution of CAF to the radical scavenging activity of one gram of whole brown rice was similar to those of alpha T, alpha T3, and gamma T3 because of its weaker antioxidant activity. The CAF pretreatment displayed a significant cytoprotective effect on the hydrogen peroxide-induced cytotoxicity from 10 mu M, which is lower than the minimal concentrations of alpha T and gamma T required for a significant protection. CAF also enhanced the nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation coincided with the enhancement of the heme oxygenase-1 (HO-1) mRNA level. An HO-1 inhibitor, tin protoporphyrin IX (SnPP), significantly impaired the cytoprotection of CAF. The cytoprotective potential of CAF is attributable to its cycloartenyl moiety besides the ferulyl moiety. These results suggested that CAF is the predominant cytoprotector in brown rice against hydrogen peroxide-induced cytotoxicity.
en-copyright=
kn-copyright=
en-aut-name=WuHongyan
en-aut-sei=Wu
en-aut-mei=Hongyan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=NakamuraToshiyuki
en-aut-sei=Nakamura
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=GuoYingnan
en-aut-sei=Guo
en-aut-mei=Yingnan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=MatsumotoRiho
en-aut-sei=Matsumoto
en-aut-mei=Riho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=MunemasaShintaro
en-aut-sei=Munemasa
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
affil-num=1
en-affil=School of Food Science and Technology, Dalian Polytechnic University
kn-affil=
affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=3
en-affil=School of Food Science and Technology, Dalian Polytechnic University
kn-affil=
affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=5
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=6
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=7
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=cycloartenyl ferulate
kn-keyword=cycloartenyl ferulate
en-keyword=antioxidative effect
kn-keyword=antioxidative effect
en-keyword=cytoprotective potential
kn-keyword=cytoprotective potential
en-keyword=heme oxygenase-1
kn-keyword=heme oxygenase-1
en-keyword=nuclear factor erythroid 2-related factor 2
kn-keyword=nuclear factor erythroid 2-related factor 2
END
start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=19
article-no=
start-page=11035
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220920
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Immune State Conversion of the Mesenteric Lymph Node in a Mouse Breast Cancer Model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Secondary lymphoid tissues, such as the spleen and lymph nodes (LNs), contribute to breast cancer development and metastasis in both anti- and pro-tumoral directions. Although secondary lymphoid tissues have been extensively studied, very little is known about the immune conversion in mesenteric LNs (mLNs) during breast cancer development. Here, we demonstrate inflammatory immune conversion of mLNs in a metastatic 4T1 breast cancer model. Splenic T cells were significantly decreased and continuously suppressed IFN-gamma production during tumor development, while myeloid-derived suppressor cells (MDSCs) were dramatically enriched. However, T cell numbers in the mLN did not decrease, and the MDSCs only moderately increased. T cells in the mLN exhibited conversion from a pro-inflammatory state with high IFN-gamma expression to an anti-inflammatory state with high expression of IL-4 and IL-10 in early- to late-stages of breast cancer development. Interestingly, increased migration of CD103(+)CD11b(+) dendritic cells (DCs) into the mLN, along with increased (1 -> 3)-beta-D-glucan levels in serum, was observed even in late-stage breast cancer. This suggests that CD103(+)CD11b(+) DCs could prime cancer-reactive T cells. Together, the data indicate that the mLN is an important lymphoid tissue contributing to breast cancer development.
en-copyright=
kn-copyright=
en-aut-name=ShigehiroTsukasa
en-aut-sei=Shigehiro
en-aut-mei=Tsukasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=UenoMaho
en-aut-sei=Ueno
en-aut-mei=Maho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=KijihiraMayumi
en-aut-sei=Kijihira
en-aut-mei=Mayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TakahashiRyotaro
en-aut-sei=Takahashi
en-aut-mei=Ryotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=UmemuraChiho
en-aut-sei=Umemura
en-aut-mei=Chiho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=TahaEman A.
en-aut-sei=Taha
en-aut-mei=Eman A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=KurosakaChisaki
en-aut-sei=Kurosaka
en-aut-mei=Chisaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=AsayamaMegumi
en-aut-sei=Asayama
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=MurakamiHiroshi
en-aut-sei=Murakami
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=FutamiJunichiro
en-aut-sei=Futami
en-aut-mei=Junichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=MasudaJunko
en-aut-sei=Masuda
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
affil-num=1
en-affil=Research Institute for Biomedical Sciences, Tokyo University of Science
kn-affil=
affil-num=2
en-affil=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Okayama University
kn-affil=
affil-num=3
en-affil=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Okayama University
kn-affil=
affil-num=4
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=5
en-affil=Division of Medical Bioengineering, Graduate School of Natural Science and Technology, Okayama University
kn-affil=
affil-num=6
en-affil=Division of Medical Bioengineering, Graduate School of Natural Science and Technology, Okayama University
kn-affil=
affil-num=7
en-affil=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Okayama University
kn-affil=
affil-num=8
en-affil=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Okayama University
kn-affil=
affil-num=9
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=10
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=11
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=12
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=13
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=breast cancer cells
kn-keyword=breast cancer cells
en-keyword=dendritic cells
kn-keyword=dendritic cells
en-keyword=mesenteric lymph node
kn-keyword=mesenteric lymph node
en-keyword=myeloid-derived suppressor cells
kn-keyword=myeloid-derived suppressor cells
END
start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=3
article-no=
start-page=1762
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220203
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Major Intestinal Catabolite of Quercetin Glycosides, 3-Hydroxyphenylacetic Acid, Protects the Hepatocytes from the Acetaldehyde-Induced Cytotoxicity through the Enhancement of the Total Aldehyde Dehydrogenase Activity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aldehyde dehydrogenases (ALDHs) are the major enzyme superfamily for the aldehyde metabolism. Since the ALDH polymorphism leads to the accumulation of acetaldehyde, we considered that the enhancement of the liver ALDH activity by certain food ingredients could help prevent alcohol-induced chronic diseases. Here, we evaluated the modulating effects of 3-hydroxyphenylacetic acid (OPAC), the major metabolite of quercetin glycosides, on the ALDH activity and acetaldehyde-induced cytotoxicity in the cultured cell models. OPAC significantly enhanced the total ALDH activity not only in mouse hepatoma Hepa1c1c7 cells, but also in human hepatoma HepG2 cells. OPAC significantly increased not only the nuclear level of aryl hydrocarbon receptor (AhR), but also the AhR-dependent reporter gene expression, though not the nuclear factor erythroid-2-related factor 2 (Nrf2)-dependent one. The pretreatment of OPAC at the concentration required for the ALDH upregulation completely inhibited the acetaldehyde-induced cytotoxicity. Silencing AhR impaired the resistant effect of OPAC against acetaldehyde. These results strongly suggested that OPAC protects the cells from the acetaldehyde-induced cytotoxicity, mainly through the AhR-dependent and Nrf2-independent enhancement of the total ALDH activity. Our findings suggest that OPAC has a protective potential in hepatocyte models and could offer a new preventive possibility of quercetin glycosides for targeting alcohol-induced chronic diseases.
en-copyright=
kn-copyright=
en-aut-name=LiuYujia
en-aut-sei=Liu
en-aut-mei=Yujia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=MyojinTakumi
en-aut-sei=Myojin
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=LiKexin
en-aut-sei=Li
en-aut-mei=Kexin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=KuritaAyuki
en-aut-sei=Kurita
en-aut-mei=Ayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=SetoMasayuki
en-aut-sei=Seto
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=MotoyamaAyano
en-aut-sei=Motoyama
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=LiuXiaoyang
en-aut-sei=Liu
en-aut-mei=Xiaoyang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=MunemasaShintaro
en-aut-sei=Munemasa
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=NakamuraToshiyuki
en-aut-sei=Nakamura
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
affil-num=1
en-affil=School of Biological Engineering, Dalian Polytechnic University
kn-affil=
affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=3
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=5
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=6
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=7
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=8
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=9
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=10
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=11
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=12
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=3-hydroxyphenylacetic acid
kn-keyword=3-hydroxyphenylacetic acid
en-keyword=aldehyde dehydrogenase
kn-keyword=aldehyde dehydrogenase
en-keyword=quercetin metabolites
kn-keyword=quercetin metabolites
en-keyword=aryl hydrocarbon receptor
kn-keyword=aryl hydrocarbon receptor
en-keyword=acetaldehyde
kn-keyword=acetaldehyde
END
start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=1
article-no=
start-page=18
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211023
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Synthesis and characterization of conductive flexible cellulose carbon nanohorn sheets for human tissue applications
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background
Conductive sheets of cellulose and carbon nanomaterials and its human skin applications are an interesting research aspect as they have potential for applications for skin compatibility. Hence it is needed to explore the effects and shed light on these applications.
Method
To fabricate wearable, portable, flexible, lightweight, inexpensive, and biocompatible composite materials, carbon nanohorns (CNHs) and hydroxyethylcellulose (HEC) were used as precursors to prepare CNH-HEC (Cnh-cel) composite sheets. Cnh-cel sheets were prepared with different loading concentrations of CNHs (10, 20 50,100mg) in 200mg cellulose. To fabricate the bio-compatible sheets, a pristine composite of CNHs and HEC was prepared without any pretreatment of the materials.
Results
The obtained sheets possess a conductivity of 1.83x10(-10)S/m and bio-compatible with human skin. Analysis for skin-compatibility was performed for Cnh-cel sheets by h-CLAT in vitro skin sensitization tests to evaluate the activation of THP-1 cells. It was found that THP-1 cells were not activated by Cnh-cel; hence Cnh-cel is a safe biomaterial for human skin. It was also found that the composite allowed only a maximum loading of 100mg to retain the consistent geometry of free-standing sheets of <100m thickness. Since CNHs have a unique arrangement of aggregates (dahlia structure), the composite is homogeneous, as verified by transmission electron microscopy (TEM) and, scanning electron microscopy (SEM), and other functional properties investigated by Raman spectroscopy, Fourier transform infrared spectroscopy (FT-IR), conductivity measurement, tensile strength measurement, and skin sensitization.
Conclusion
It can be concluded that cellulose and CNHs sheets are conductive and compatible to human skin applications.
en-copyright=
kn-copyright=
en-aut-name=SelvamKarthik Paneer
en-aut-sei=Selvam
en-aut-mei=Karthik Paneer
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=NagahataTaichi
en-aut-sei=Nagahata
en-aut-mei=Taichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=KatoKosuke
en-aut-sei=Kato
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=NakamuraToshiyuki
en-aut-sei=Nakamura
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=NishikawaTakeshi
en-aut-sei=Nishikawa
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=HayashiYasuhiko
en-aut-sei=Hayashi
en-aut-mei=Yasuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
affil-num=2
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=4
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=5
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=6
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=7
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
affil-num=8
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=9
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Carbon Nanohorns
kn-keyword=Carbon Nanohorns
en-keyword=Cellulose
kn-keyword=Cellulose
en-keyword=Skin sensitization
kn-keyword=Skin sensitization
en-keyword=Composites
kn-keyword=Composites
en-keyword=Bio-compatible
kn-keyword=Bio-compatible
END
start-ver=1.4
cd-journal=joma
no-vol=71
cd-vols=
no-issue=10
article-no=
start-page=2922
end-page=2932
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200227
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Inhibition of light-induced stomatal opening by allyl isothiocyanate does not require guard cell cytosolic Ca2+ signaling
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The glucosinolate-myrosinase system is a well-known defense system that has been shown to induce stomatal closure in Brassicales. Isothiocyanates are highly reactive hydrolysates of glucosinolates, and an isothiocyanate, allyl isothiocyanate (AITC), induces stomatal closure accompanied by elevation of free cytosolic Ca2+ concentration ([Ca2+](cyt)) in Arabidopsis. It remains unknown whether AITC inhibits light-induced stomatal opening. This study investigated the role of Ca2+ in AITC-induced stomatal closure and inhibition of light-induced stomatal opening. AITC induced stomatal closure and inhibited light-induced stomatal opening in a dose-dependent manner. A Ca2+ channel inhibitor, La3+, a Ca(2+)chelator, EGTA, and an inhibitor of Ca2+ release from internal stores, nicotinamide, inhibited AITC-induced [Ca2+](cyt) elevation and stomatal closure, but did not affect inhibition of light-induced stomatal opening. AITC activated non-selective Ca2+-permeable cation channels and inhibited inward-rectifying K+ (K-in(+)) channels in a Ca2+-independent manner. AITC also inhibited stomatal opening induced by fusicoccin, a plasma membrane H+-ATPase activator, but had no significant effect on fusicoccin-induced phosphorylation of the penultimate threonine of H+-ATPase. Taken together, these results suggest that AITC induces Ca2+ influx and Ca2+ release to elevate [Ca2+](cyt), which is essential for AITC-induced stomatal closure but not for inhibition of K-in(+) channels and light-induced stomatal opening.
en-copyright=
kn-copyright=
en-aut-name=YeWenxiu
en-aut-sei=Ye
en-aut-mei=Wenxiu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=AndoEigo
en-aut-sei=Ando
en-aut-mei=Eigo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=RhamanMohammad Saidur
en-aut-sei=Rhaman
en-aut-mei=Mohammad Saidur
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=Tahjib-Ul-ArifMd
en-aut-sei=Tahjib-Ul-Arif
en-aut-mei=Md
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=OkumaEiji
en-aut-sei=Okuma
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=KinoshitaToshinori
en-aut-sei=Kinoshita
en-aut-mei=Toshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=2
en-affil=Graduate School of Science, Nagoya University
kn-affil=
affil-num=3
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=5
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=6
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=7
en-affil=Institute of Transformative Bio-Molecule, Nagoya University
kn-affil=
affil-num=8
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=Allyl isothiocyanate
kn-keyword=Allyl isothiocyanate
en-keyword=Arabidopsis
kn-keyword=Arabidopsis
en-keyword=calcium channel
kn-keyword=calcium channel
en-keyword=potassium channel
kn-keyword=potassium channel
en-keyword=proton pump
kn-keyword=proton pump
en-keyword=stomatal closure
kn-keyword=stomatal closure
en-keyword=stomatal opening
kn-keyword=stomatal opening
END
start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=
article-no=
start-page=8866
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=2019620
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Yeast screening system reveals the inhibitory mechanism of cancer cell proliferation by benzyl isothiocyanate through down-regulation of Mis12
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Benzyl isothiocyanate (BITC) is a naturally-occurring isothiocyanate derived from cruciferous vegetables. BITC has been reported to inhibit the proliferation of various cancer cells, which is believed to be important for the inhibition of tumorigenesis. However, the detailed mechanisms of action remain unclear. In this study, we employed a budding yeast Saccharomyces cerevisiae as a model organism for screening. Twelve genes including MTW1 were identified as the overexpression suppressors for the antiproliferative effect of BITC using the genome-wide multi-copy plasmid collection for S. cerevisiae. Overexpression of the kinetochore protein Mtw1 counteracts the antiproliferative effect of BITC in yeast. The inhibitory effect of BITC on the proliferation of human colon cancer HCT-116 cells was consistently suppressed by the overexpression of Mis12, a human orthologue of Mtw1, and enhanced by the knockdown of Mis12. We also found that BITC increased the phosphorylated and ubiquitinated Mis12 level with consequent reduction of Mis12, suggesting that BITC degrades Mis12 through an ubiquitin-proteasome system. Furthermore, cell cycle analysis showed that the change in the Mis12 level affected the cell cycle distribution and the sensitivity to the BITC-induced apoptosis. These results provide evidence that BITC suppresses cell proliferation through the post-transcriptional regulation of the kinetochore protein Mis12.
en-copyright=
kn-copyright=
en-aut-name=Abe-KanohNaomi
en-aut-sei=Abe-Kanoh
en-aut-mei=Naomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=KunisueNarumi
en-aut-sei=Kunisue
en-aut-mei=Narumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=MyojinTakumi
en-aut-sei=Myojin
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=ChinoAyako
en-aut-sei=Chino
en-aut-mei=Ayako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=MunemasaShintaro
en-aut-sei=Munemasa
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=MoriyaHisao
en-aut-sei=Moriya
en-aut-mei=Hisao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=3
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=4
en-affil=Research Core for Interdisciplinary Sciences, Okayama University
kn-affil=
affil-num=5
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=6
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=7
en-affil= Graduate School of Natural Science and Technology, Okayama University
kn-affil=
affil-num=8
en-affil=Research Core for Interdisciplinary Sciences, Okayama University
kn-affil=
affil-num=9
en-affil=Graduate School of Environmental and Life Science, Okayama University, Okayama
kn-affil=
END
start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=
article-no=
start-page=160
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190827
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Golgin Protein Giantin Regulates Interconnections Between Golgi Stacks
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Golgins are a family of Golgi-localized long coiled-coil proteins. The major golgin function is thought to be the tethering of vesicles, membranes, and cytoskeletal elements to the Golgi. We previously showed that knockdown of one of the longest golgins, Giantin, altered the glycosylation patterns of cell surfaces and the kinetics of cargo transport, suggesting that Giantin maintains correct glycosylation through slowing down transport within the Golgi. Giantin knockdown also altered the sizes and numbers of mini Golgi stacks generated by microtubule de-polymerization, suggesting that it maintains the independence of individual Golgi stacks. Therefore, it is presumed that Golgi stacks lose their independence following Giantin knockdown, allowing easier and possibly increased transport among stacks and abnormal glycosylation. To gain structural insights into the independence of Golgi stacks, we herein performed electron tomography and 3D modeling of Golgi stacks in Giantin knockdown cells. Compared with control cells, Giantin-knockdown cells had fewer and smaller fenestrae within each cisterna. This was supported by data showing that the diffusion rate of Golgi membrane proteins is faster in Giantin-knockdown Golgi, indicating that Giantin knockdown structurally and functionally increases connectivity among Golgi cisternae and stacks. This increased connectivity suggests that contrary to the cis-golgin tether model, Giantin instead inhibits the tether and fusion of nearby Golgi cisternae and stacks, resulting in transport difficulties between stacks that may enable the correct glycosylation of proteins and lipids passing through the Golgi.
en-copyright=
kn-copyright=
en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=Hayashi-NishinoMitsuko
en-aut-sei=Hayashi-Nishino
en-aut-mei=Mitsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=ShakunoTakuto
en-aut-sei=Shakuno
en-aut-mei=Takuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=MasudaJunko
en-aut-sei=Masuda
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=MurakamiRuna
en-aut-sei=Murakami
en-aut-mei=Runa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=NakamuraToshiyuki
en-aut-sei=Nakamura
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=Abe-KanohNaomi
en-aut-sei=Abe-Kanoh
en-aut-mei=Naomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=HonjoYasuko
en-aut-sei=Honjo
en-aut-mei=Yasuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=MalsamJoerg
en-aut-sei=Malsam
en-aut-mei=Joerg
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=YuSidney
en-aut-sei=Yu
en-aut-mei=Sidney
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=ishinoKunihiko
en-aut-sei=ishino
en-aut-mei=Kunihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=2
en-affil=Institute of Scientific and Industrial Research, Osaka University
kn-affil=
affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
affil-num=4
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=5
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=6
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
affil-num=7
en-affil=raduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=8
en-affil=raduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=9
en-affil=raduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=10
en-affil=esearch Institute for Radiation Biology and Medicine, Hiroshima University
kn-affil=
affil-num=11
en-affil=Center for Biochemistry (BZH), Heidelberg University
kn-affil=
affil-num=12
en-affil=School of Biomedical Sciences, The Chinese University of Hong Kong
kn-affil=
affil-num=13
en-affil=Institute of Scientific and Industrial Research, Osaka University
kn-affil=
en-keyword=Golgi
kn-keyword=Golgi
en-keyword=golgins
kn-keyword=golgins
en-keyword=glycosylation
kn-keyword=glycosylation
en-keyword=endoplasmic reticulum
kn-keyword=endoplasmic reticulum
en-keyword=electron tomography
kn-keyword=electron tomography
END
start-ver=1.4
cd-journal=joma
no-vol=57
cd-vols=
no-issue=8
article-no=
start-page=1779
end-page=1990
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20160801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Involvement of OST1 Protein Kinase and PYR/PYL/RCAR Receptors in Methyl Jasmonate-Induced Stomatal Closure in Arabidopsis Guard Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Methyl jasmonate (MeJA) induces stomatal closure. It has been shown that stomata of many ABA-insensitive mutants are also insensitive to MeJA, and a low amount of ABA is a prerequisite for the MeJA response. However, the molecular mechanisms of the interaction between ABA and MeJA signaling remain to be elucidated. Here we studied the interplay of signaling of the two hormones in guard cells using the quadruple ABA receptor mutant pyr1 pyl1 pyl2 pyl4 and ABA-activated protein kinase mutants ost1-2 and srk2e. In the quadruple mutant, MeJA-induced stomatal closure, H2O2 production, nitric oxide (NO) production, cytosolic alkalization and plasma membrane Ca(2+)-permeable current (ICa) activation were not impaired. At the same time, the inactivation of the inward-rectifying K(+) current was impaired. In contrast to the quadruple mutant, MeJA-induced stomatal closure, H2O2 production, NO production and cytosolic alkalization were impaired in ost1-2 and srk2e as well as in aba2-2, the ABA-deficient mutant. The activation of ICa was also impaired in srk2e. Collectively, these results indicated that OST1 was essential for MeJA-induced stomatal closure, while PYR1, PYL1, PYL2 and PYL4 ABA receptors were not sufficient factors. MeJA did not appear to activate OST1 kinase activity. This implies that OST1 mediates MeJA signaling through an undetectable level of activity or a non-enzymatic action. MeJA induced the expression of an ABA synthesis gene, NCED3, and increased ABA contents only modestly. Taken together with previous reports, this study suggests that MeJA signaling in guard cells is primed by ABA and is not brought about through the pathway mediated by PYR1, PYL1 PYL2 and PYL4.
en-copyright=
kn-copyright=
en-aut-name=YinYe
en-aut-sei=Yin
en-aut-mei=Ye
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=AdachiYuji
en-aut-sei=Adachi
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=MunemasaShintaro
en-aut-sei=Munemasa
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=MoriIzumi C.
en-aut-sei=Mori
en-aut-mei=Izumi C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=3
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
affil-num=5
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
affil-num=6
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=ABA
kn-keyword=ABA
en-keyword=ABA receptors
kn-keyword=ABA receptors
en-keyword=Arabidopsis thaliana
kn-keyword=Arabidopsis thaliana
en-keyword=Guard cells
kn-keyword=Guard cells
en-keyword=Methyl jasmonate
kn-keyword=Methyl jasmonate
en-keyword=OST1 protein kinase
kn-keyword=OST1 protein kinase
END
start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20141120
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Nuclear factor-kappaB sensitizes to benzyl isothiocyanate-induced antiproliferation in p53-deficient colorectal cancer cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Benzyl isothiocyanate (BITC), a dietary isothiocyanate derived from cruciferous vegetables, inhibits the proliferation of colorectal cancer cells, most of which overexpress β-catenin as a result of mutations in the genes for adenomatous polyposis coli or mutations in β-catenin itself. Because nuclear factor-κB (NF-κB) is a plausible target of BITC signaling in inflammatory cell models, we hypothesized that it is also involved in BITC-inhibited proliferation of colorectal cancer cells. siRNA-mediated knockdown of the NF-κB p65 subunit significantly decreased the BITC sensitivity of human colorectal cancer HT-29 cells with mutated p53 tumor suppressor protein. Treating HT-29 cells with BITC induced the phosphorylation of IκB kinase, IκB-α and p65, the degradation of IκB-α, the translocation of p65 to the nucleus and the upregulation of NF-κB transcriptional activity. BITC also decreased β-catenin binding to a positive cis element of the cyclin D1 promoter and thus inhibited β-catenin-dependent cyclin D1 transcription, possibly through a direct interaction between p65 and β-catenin. siRNA-mediated knockdown of p65 confirmed that p65 negatively affects cyclin D1 expression. On the other hand, when human colorectal cancer HCT-116 cells with wild-type p53 were treated with BITC, translocation of p65 to the nucleus was inhibited rather than enhanced. p53 knockout increased the BITC sensitivity of HCT-116 cells in a p65-dependent manner, suggesting that p53 negatively regulates p65-dependent effects. Together, these results identify BITC as a novel type of antiproliferative agent that regulates the NF-κB pathway in p53-deficient colorectal cancer cells.
en-copyright=
kn-copyright=
en-aut-name=AbeN
en-aut-sei=Abe
en-aut-mei=N
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=HouD-X
en-aut-sei=Hou
en-aut-mei=D-X
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=MunemasaS
en-aut-sei=Munemasa
en-aut-mei=S
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=MurataY
en-aut-sei=Murata
en-aut-mei=Y
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=NakamuraY
en-aut-sei=Nakamura
en-aut-mei=Y
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
affil-num=1
en-affil=
kn-affil=Graduate School of Environmental and Life Science, Okayama University
affil-num=2
en-affil=
kn-affil=Department of Biochemical Science and Technology, Faculty of Agriculture, Kagoshima University
affil-num=3
en-affil=
kn-affil=Graduate School of Environmental and Life Science, Okayama University
affil-num=4
en-affil=
kn-affil=Graduate School of Environmental and Life Science, Okayama University
affil-num=5
en-affil=
kn-affil=Graduate School of Environmental and Life Science, Okayama University
END
start-ver=1.4
cd-journal=joma
no-vol=95
cd-vols=
no-issue=1
article-no=
start-page=87
end-page=91
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=200602
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Isothiocyanates as Novel Cancer Chemopreventive Agents and Their Underlying Molecular Mechanisms
kn-title=イソチオシアネートによるがんの化学予防の可能性
en-subtitle=
kn-subtitle=
en-abstract=野菜全般の摂取と健康状態に関する疫学的研究は，近年数多く報告されており，様々な疾患リスクの低減だけでなく，通常の健康状態に関しても野菜の有効・有用性が示唆されている．その一方で，食生活の欧米化の着実な進行から，肉食・魚介類の順調な消費の伸びに対し，野菜消費量が減少の一途を辿っている．特に，若年齢層を中心とした世代の野菜消費量の減少が顕著であり，生活習慣病の若年齢化との相関から，社会問題として注目を浴びつつある．例えば，野菜を十分に摂取出来れば所要量の確保が容易なビタミンである葉酸であるが，新生児の神経管閉鎖障害症の最近の増加から，妊娠初期の女性の摂取不足に厚生労働省が警鐘を鳴らしている．また，昨今の栄養・健康情報の氾濫とサプリメント（栄養補助食品，健康補助食品）市場の急激な成長により，サプリメントを利用しておけば普段の食生活はないがしろにしても構わないという風潮に歯止めがかからなくなっている．野菜の摂取を推奨していくためには，人の健康と野菜摂取との関連を科学的かつ体系的に解明・整理にすることが今一度必要である．野菜中に含まれる，より具体的な機能性成分の性質や分布を正確に理解し，健康維持や疾病予防への寄与を明らかにすることができれば，より健全な「日本型食生活」への回帰を目指した野菜の消費拡大の一助となることはいうまでもない．それゆえ，これからの食品機能の基盤的研究が果たす役割は極めて重要であるといえる．食品機能の基盤的研究のなかで，現在最も体系的に進んでいる研究分野として，がん予防に関する研究が挙げられる．発がんの原因物質の排除と発がん抑制物質の積極的な摂取が「がんの化学予防」の基本戦略であるが，数多くの疫学的研究や動物実験の成果から，野菜や果物などの植物性食品の摂取が予防に有効であるといわれて久しい．特に，1990年代に米国で「デザイナーフーズ」計画がスタートしたことをきっかけとして，十数余年にわたるこれまでの研究は，がん予防に有望な素材・成分の化学的解明，動物実験成績や基本的作用機構に関する知見の蓄積だけでなく，その他の疾病をターゲットとし
た食品機能研究の進展に大きく寄与してきた．その一方で，β-カロテンのヒト介入試験での不成功から，食品成分による疾病予防法確立への道は決して平坦なものではないことも浮彫りとなった．現在，がんの化学予防研究は，ヒトにおける有効性をどのように評価して行くかを共通課題とし，体内動態や遺伝子発現の網羅的，体系的解析などのより詳細な分子レベルでの研究へと進展を遂げつつあり，筆者も例に漏れず研究標的をシフトしてきた．また，これまで有効とされてきた素材・成分の再評価，品種改良などによる有効成分（活性及び含量の）増強素材の開発，より偏りの少ない食事・栄養指導など，網羅すべき課題の広がりにより，食品化学分野は新展開の局面を迎えている
kn-abstract=A promising group of compounds that have a chemopreventive property are isothiocyanates (ITCs). ITCs have been shown to induce apoptosi in various cancer cell lines and experimental rodents. Multiple signaltransduction pathways as well as apoptosis intermediates have been also posturalted. We recently clarified the moleculae mechanism underlying the relationship between cell cycle arrest ad apoptosis induced by benzyl isothiocyanate(BITC), a major ITC compound isolated from papaya. The exposure of cells to BITC resulted in the inhibition of the G2/M progression that coincided with not only hte up-regulated expression of the G2/M cell cycle arrest-regulating genes but also the apoptosis induction. Conversely, treatment with an excessive concentration of BITC resulted in an abortive apoptotic pathway without DNA ladder formation. This commentary will review the biological impact of cell death induction by BITC as well as other ITCs and the involved signal transduction pathways.
en-copyright=
kn-copyright=
en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=中村宣督
kn-aut-sei=中村
kn-aut-mei=宣督
aut-affil-num=1
ORCID=
affil-num=1
en-affil=
kn-affil=岡山大学
en-keyword=isothiocyanates
kn-keyword=isothiocyanates
en-keyword=cancer chemoprevention
kn-keyword=cancer chemoprevention
en-keyword=apoptosis
kn-keyword=apoptosis
en-keyword=cell cycle arrest
kn-keyword=cell cycle arrest
en-keyword=necrosis
kn-keyword=necrosis
END