| Project/Area Number |
26461129
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Osaka University |
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Principal Investigator |
Hikoso Shungo 大阪大学, 医学系研究科, 寄附講座准教授 (30423164)
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| Co-Investigator(Kenkyū-buntansha) |
山口 修 大阪大学, 医学系研究科, 准教授 (90467580)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | DNase II / 心不全 / 遺伝子改変マウス / iPS細胞 |
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| Outline of Final Research Achievements |
We investigated the role of DNase II, which is a responsible molecule for degradation of mitochondrial DNA, in the pathogenesis of heart failure. As for the regulatory mechanism of DNase activity, we identified that the activity is regulated via post-translational mechanism, and now we are investigating the detail. As for the therapeutic implication of DNase II for heart failure, we created cardiac-specific DNase II transgenic mice, and evaluated the phenotype. In addition, we evaluated the role of DNase II in human heart failure pathophysiology using human cardiac tissue sample of heart failure patients, and found that the expression of DNase II in failing heart is decreased compared with non-failing heart. We also found that DNA is deposited in cardiomyocytes in patients with heart failure.
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