| Project/Area Number |
22790693
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
TANAKA Hirotoshi 東京大学, 医科学研究所, 准教授 (00171794)
SHIMIZU Noriaki 東京大学, 医科学研究所, 特任研究員 (30396890)
SANO Motoaki 慶應義塾大学, 医学部, 講師 (30265798)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 心肥大 / 心臓リモデリング / 心不全 / HEXIM1 / 転写伸長反応 / P-TEFb / RNAポリメラーゼII / 右心肥大 / 肺高血圧症 / 心筋リモデリング |
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| Research Abstract |
[Objectives] Because HEXIM is the only molecule to inhibit P-TEFb, which is the key molecule for development of cardiac hypertrophy, we speculate that HEXIM1 may be a candidate for preventing cardiac hypertrophy/remodeling.[ Methods and Results] Using adenovirus mediated gene delivery to the cultured cardiac myocytes and a new transgenic mouse model with conditional myocardial overexpression of HEXIM1, we confirmed that overexpression of HEXIM1 in the cardiac myocytes prevents cardiac myocyte hypertrophy both in vitro and in vivo.[ Conclusion] HEXIM1 may be a candidate for preventing cardiac hypertrophy/remodeling.
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