Pathophysiological roles of alphaB crytallin in the failing heart floowing myocardial infarction and its therapy
| Project/Area Number |
23590115
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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 |
Biological pharmacy
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 心不全 / 熱ショックタンパク質 / ミトコンドリア / 心筋梗塞 / 心機能 / アミロイドオリゴマー / 循環器疾患 / ストレス / クリスタリン / 低分子量熱ショックタンパク質 |
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| Research Abstract |
Pathophysiological role of alphaB crystallin (CryAB) in the development of heart failure following myocardial infarction in rats was examined. Signs of chronic heart failure 8 weeks after the left coronary artery ligation in rats were seen. CryAB content in the viable left ventricle at the 2nd week after myocardial infarction tended to be increased. In contrast, CryAB content in the viable left ventricle was similar to that in the normal myocardium. An inactive form of heat shock factor-1 (HSF-1) was increased in the failing heart. The HSF-1 inactivation also resulted in a failure of HSP72 induction after an exposure to stress. An activated CryAB in mitochondria of the failing heart was reduced. When treatment with geranylgeranylacetone increased activated CryAB in myocardial mitochondria, mitochondrial energy producing ability was preserved. These results suggest that prevention of HSF-1 and CryAB activation involves in the development of heart failure following myocardial infarction.
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Report
(4 results)
Research Products
(15 results)
