| Project/Area Number |
26282122
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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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) |
毛利 聡 川崎医科大学, 医学部, 教授 (00294413)
金川 基 神戸大学, 医学(系)研究科(研究院), 講師 (00448044)
片野坂 公明 中部大学, 公私立大学の部局等, 准教授 (50335006)
中村 一文 岡山大学, 医歯(薬)学総合研究科, 准教授 (10335630)
氏原 嘉洋 川崎医科大学, 医学部, 助教 (80610021)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,510,000 (Direct Cost: ¥12,700,000、Indirect Cost: ¥3,810,000)
Fiscal Year 2016: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2014: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Keywords | メカノセンサー / 心筋細胞 / リモデリング / カルシウム / チャネル / 血行動態負荷 / 心肥大 / 心不全 / 心臓 / 循環器・高血圧 / 生理学 / タンパク質 / 遺伝子 / トランスレーショナルリサーチ / メカニカルストレス / 血行動態 / 高血圧 / 分子生理 |
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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. Here we generated temporally-controlled cardiac-specific transient receptor potential, vanilloid family type 2 (TRPV2)-deficient mice. The elimination of cardiac TRPV2 resulted in a rapid and severe decline in cardiac function, with abnormal cellular morphology, intracellular Ca2+ handling, and contractility. These results suggested that TRPV2 is critical for the maintenance of cardiac structure and function.
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