| Project/Area Number |
24659131
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
General medical chemistry
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| Research Institution | Kyoto University |
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Principal Investigator |
YAMAZAKI Daiju 京都大学, 生理化学ユニット, 講師 (40467428)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | TRICチャネル / 心臓線維化 / イソプロテレノール / 心筋細胞死 / ネクローシス / TRIC-A |
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| Research Abstract |
TRIC-A is abundantly expressed in excitable tissues. Cardiac fibrosis was significantly induced by chronic beta-adrenergic receptor stimulation (Isoproterenol, Iso) in Tric-a-knockout mice. In this study, to investigate the underlying mechanisms, we focused on cardiomyocyte death. Elevated serum troponin T level and increased membrane permeability of evans blue dye which means cardiomyocyte necrosis induced by isoproterenol stimulation were detected in Tric-a-knockout mice. Moreover mitochondrial dysfunction was observed in Iso-stimulated Tric-a-knockout heart under electron microscopic examination.
Thus, it is suggested that remarkable cardiomyocyte necrosis is at least in part related to Iso-induced cardiac fibrosis in Tric-a-knockout mice.
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