| Project/Area Number |
22590244
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Kumamoto University |
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Principal Investigator |
YORINAKA Hoichi (LAI Zhong-fang) 熊本大学, 生命科学研究部, 助教 (90244110)
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| Co-Investigator(Kenkyū-buntansha) |
YORINAKA Gyokuchin 熊本大学, 生命科学研究部, 産学官連携研究員 (50418828)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | TNNI3K / 心筋トロポニン I / 遺伝子機能 / ELISA / 心筋細胞分化 / 心筋トロポニンI / 不整脈 / 遺伝子導入 / 抗TNNI3Kポリクローナル抗体 / MAPキナーゼ / 心筋トロポニンI(cTnI) / 心筋細胞の拍動頻度 / 抗TNNI3K抗体 / 急性心筋梗塞 / 血中TNNI3K濃度 |
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| Research Abstract |
TNNI3K is a MAP kinase specifically and continuouslyexpressed in cardiac muscle and interacted with cardiac troponin I (TNNI3, or: cTnI). The aim of this study is to investigate role of TNNI3K interacting with cTnI on modification the physiological function of cardiomyocytes, suppressing some pathological injuries and to explain the new molecular mechanism for TNNI3K-mutant in the ischemic coronary heart diseases, and hope to develop some new therapeutic strategies. In the in vitro experiments, 1) Effects of PKC inhibitor (GF109203X) or PKA activator (Br-8-cAMP) on the beating frequency were investigated in P19CL6-derived culture beating cardiomyocytes. Results showed that TNNI3K-overexpression increased the contractility and beating frequency together with restrained phosphorylation of cTnI through activation of the PKA pathway but not by blocking of the PKC pathway. 2) Availability of plasma TNNI3K level was investigated using with anti-TNNI3K poly-antibodies in patients diagnosed as AMI (n=40), chronic heart failure (CHF, n=18) and acute renal failure (ARF, n=6); and in healthy volunteers (n=12). Data shown that circulating TNNI3K levels were significantly higher in AMI (p
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