| Project/Area Number |
25860613
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | Phosphodiesterase / Angiotensin II / Isoproterenol / 酸化ストレス / ホスホジエステラーぜ / 心筋線維化 / 心筋肥大 / TGF-β / 虚血再灌流障害 |
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| Outline of Final Research Achievements |
We used cardiospecific PDE3A overexpression (PDE3TG) mice to the study. Ischemia-reperfusion injury was subjected to PDE3TG or wild-type (WT) mice. PDE3TG mice showed smaller myocardial infarction area than WT mice. A number of apoptotic cariomyocytes were lower in PDE3TG mice. We also performed angiotensin II stimulation. PDE3TG mice displayed inhibited cardiac hypertrophy and fibrosis compared to WT mice. The expression levels of transforming growth factor β, which was increased in WT mice after angiotensin II stimulation, was inhibited in PDE3TG mice. Finally we performed Isoproterenol stimulation. PDE3TG mice showed inhibited cardiac hypertrophy compared to WT mice. 8-OHDG positive area, which indicates oxidative damage, was increased in WT mice heart after isoproterenol stimulation, but not in PDE3TG mice heart. Sirt1 protein expression levels were increased in PDE3TG heart. Thus, we conclude PDE3A has cardioprotective effects through various mechanisms.
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