| 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 |
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| Research Field |
Biomedical engineering/Biomaterial science and engineering
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| Research Institution | Okayama University |
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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)
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| 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 |
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| 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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