The maintenance of cardiac structure and function by mechanical feedback system involving multiple organ systems.
Project/Area Number |
26560211
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Biomedical engineering/Biomaterial science and engineering
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Research Institution | Okayama University |
Principal Investigator |
Katanosaka Yuki 岡山大学, 医歯(薬)学総合研究科, 助教 (60432639)
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Co-Investigator(Kenkyū-buntansha) |
UJIHARA Yoshihiro 川崎医科大学, 医学部, 助教 (80610021)
MOHRI Satoshi 川崎医科大学, 医学部, 教授 (00294413)
KATANOSAKA Kimiaki 中部大学, 生命健康学科, 准教授 (50335006)
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Project Period (FY) |
2014-04-01 – 2016-03-31
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Project Status |
Completed (Fiscal Year 2015)
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Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | メカノセンサー / TRPV2 / ノックアウトマウス / 心臓 / 心筋細胞 / 心機能 / 微細構造 / 細胞骨格 / 骨格筋 / 血管 / カルシウム / 分子生理 / 分子機能評価 / 心不全 |
Outline of Final Research Achievements |
The heart has a dynamic compensatory mechanism for haemodynamic stress. However, the molecular details of myocardial mechanotransduction have remained unclear. Recently, we generated the several types of tissue-specific TRPV2-deficient mice. Elimination of TRPV2 from mouse hearts showed severe cardiac dysfunction, with disorganization of the intercalated discs that support mechanical coupling with neighbouring myocytes and myocardial conduction defects. These results suggested that TRPV2 is critical for the maintenance of cardiac structure and function in the basal state and in response to haemodynamic stress. In addition, several types of tissue-specific TRPV2-deficient mice also showed cardiac dysfunction and morphological abnormality. Therefore, cardiac morphology and function is maintained by mechanical feedback system involving multiple-organ system.
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Report
(3 results)
Research Products
(20 results)
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[Journal Article] TRPV2 is critical for the maintenance of cardiac structure and function in mice.2014
Author(s)
Katanosaka Y, Iwasaki K, Ujihara Y, Takatsu S, Nishitsuji K, Kanagawa M, Sudo A, Toda T, Katanosaka K, Mohri S, Naruse K.
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Journal Title
Nat Comm
Volume: 5
Issue: 1
Pages: 3932-3932
DOI
NAID
Related Report
Peer Reviewed / Open Access
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[Journal Article] Overexpression of LARGE suppresses muscle regeneration via down-regulation of insulin like growth factor 1 and aggravates muscular dystrophy in mice.2014
Author(s)
Saito F, Kanagawa M, Ikeda M, Hagiwara H, Masaki T, Ohkuma H, Katanosaka Y, Shimizu T, Sonno M, Toda T, Matsumura K.
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Journal Title
Hum Mol Genet.
Volume: 23
Pages: 4553-4558
Related Report
Peer Reviewed
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[Journal Article] Involvement of S1P1 receptor pathway in angiogeniceffects of a novel adenosine-like nucleic acid analog COA-Cl in cultured human vascular endothelial cells.2014
Author(s)
Junsuke Igarashi, Takeshi Hashimoto, Yasuo Kubota, Kazuyo Shoji, Tokumi Maruyama, Norikazu Sakakibara, Yoh Takuwa, Yoshihiro Ujihara, Yuki Katanosaka, Satoshi Mohri, Keiji Naruse, Tetsuo Yamashita, Ryuji Okamoto, Katsuya Hirano, Hiroaki Kosaka, Maki Takata,Ryoji Konishi, Ikuko Tsukamoto.
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Journal Title
Pharmacology Research and Perspectives
Volume: -
Related Report
Peer Reviewed
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