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TRPC3 positively regulates reactive oxygen species driving maladaptive cardiac remodeling
http://hdl.handle.net/10091/00021005
http://hdl.handle.net/10091/000210054c90dc70-8930-4e56-a2c6-ab12cccd0df1
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
srep37001.pdf (2.8 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2018-10-31 | |||||
| タイトル | ||||||
| タイトル | TRPC3 positively regulates reactive oxygen species driving maladaptive cardiac remodeling | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| DOI | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | https://doi.org/10.1038/srep37001 | |||||
| 関連名称 | 10.1038/srep37001 | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | Cardiac hypertrophy | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | Ion channel signalling | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Kitajima, Naoyuki
× Kitajima, Naoyuki× Numaga-Tomita, Takuro× Watanabe, Masahiko× Kuroda, Takuya× Nishimura, Akiyuki× Miyano, Kei× Yasuda, Satoshi× Kuwahara, Koichiro× Sato, Yoji× Ide, Tomomi× Birnbaumer, Lutz× Sumimoto, Hideki× Mori, Yasuo× Nishida, Motohiro |
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| 信州大学研究者総覧へのリンク | ||||||
| 表示名 | Kuwahara, Koichiro | |||||
| URL | http://soar-rd.shinshu-u.ac.jp/profile/ja.HVchWCcp.html | |||||
| 出版者 | ||||||
| 出版者 | NATURE PUBLISHING GROUP | |||||
| 引用 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | SCIENTIFIC REPORTS. 6: 37001(2016) | |||||
| 書誌情報 |
SCIENTIFIC REPORTS 巻 6, p. 37001, 発行日 2016-11-11 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Reactive oxygen species (ROS) produced by NADPH oxidase 2 (Nox2) function as key mediators of mechanotransduction during both physiological adaptation to mechanical load and maladaptive remodeling of the heart. This is despite low levels of cardiac Nox2 expression. The mechanism underlying the transition from adaptation to maladaptation remains obscure, however. We demonstrate that transient receptor potential canonical 3 (TRPC3), a Ca2+-permeable channel, acts as a positive regulator of ROS (PRROS) in cardiomyocytes, and specifically regulates pressure overload-induced maladaptive cardiac remodeling in mice. TRPC3 physically interacts with Nox2 at specific C-terminal sites, thereby protecting Nox2 from proteasome-dependent degradation and amplifying Ca2+-dependent Nox2 activation through TRPC3-mediated background Ca2+ entry. Nox2 also stabilizes TRPC3 proteins to enhance TRPC3 channel activity. Expression of TRPC3 C-terminal polypeptide abolished TRPC3-regulated ROS production by disrupting TRPC3-Nox2 interaction, without affecting TRPC3-mediated Ca2+ influx. The novel TRPC3 function as a PRROS provides a mechanistic explanation for how diastolic Ca2+ influx specifically encodes signals to induce ROS-mediated maladaptive remodeling and offers new therapeutic possibilities. | |||||
| 資源タイプ（コンテンツの種類） | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Article | |||||
| ISSN | ||||||
| 収録物識別子タイプ | EISSN | |||||
| 収録物識別子 | 2045-2322 | |||||
| PubMed | ||||||
| 識別子タイプ | PMID | |||||
| 関連識別子 | https://www.ncbi.nlm.nih.gov/pubmed/27833156 | |||||
| 関連名称 | 27833156 | |||||
| 権利 | ||||||
| 権利情報 | 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/ | |||||
| 出版タイプ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
| WoS | ||||||
| 表示名 | Web of Science | |||||
| URL | http://gateway.isiknowledge.com/gateway/Gateway.cgi?&GWVersion=2&SrcAuth=ShinshuUniv&SrcApp=ShinshuUniv&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000387476100001 | |||||
