ID | 53904 |
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Katanosaka, Yuki
Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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Iwasaki, Keiichiro
Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Ujihara, Yoshihiro
Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Takatsu, Satomi
Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Nishitsuji, Koki
Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Kanagawa, Motoi
Division of Neurology/Molecular Brain Science, Kobe University Graduate School of Medicine
Sudo, Atsushi
Division of Neurology/Molecular Brain Science, Kobe University Graduate School of Medicine
Toda, Tatsushi
Division of Neurology/Molecular Brain Science, Kobe University Graduate School of Medicine
Katanosaka, Kimiaki
Department of Neuroscience II, Research Institute of Environmental Medicine, Nagoya University
Mohri, Satoshi
Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Naruse, Keiji
Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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抄録 | 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.
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備考 | This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/
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発行日 | 2014-05-29
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出版物タイトル |
Nature Communications
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巻 | 5巻
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出版者 | Nature Publishing Group
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開始ページ | 3932
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ISSN | 2041-1723
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NCID | AA12645905
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資料タイプ |
学術雑誌論文
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オフィシャル URL | http://dx.doi.org/10.1038/ncomms4932
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関連URL | http://ousar.lib.okayama-u.ac.jp/metadata/53904
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言語 |
英語
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著作権者 | © 2014 Macmillan Publishers Limited. All rights reserved. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
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論文のバージョン | publisher
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査読 |
有り
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