| Project/Area Number |
13672306
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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 |
Biological pharmacy
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
TANONAKA Kouichi Tokyo University of Pharmacy and Life Science, Department of Pharmacology, Assistant professor, 薬学部, 講師 (50188398)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Heart failure / Heat shock proteins / Stress / Mitochondria / Energy production / Cardiac function / 熱ショックタンパク質 / 細胞防御機構 / 心収縮不全 / Hsp27 / Hsp72 / Hsp60 / エネルギー代謝 |
|---|
| Research Abstract |
Effects of changes in heat shock protein of the rat failing heart following acute myocardial infarction were examined. Eight weeks after myocardial infarction, hemodynamic parameters showed symptoms of heart failure with low cardiac output. In the present study, it has been shown that an excess activation of poly(ADP-ribose) synthetase may be attenuated by Hsp70, which is translocated from cytosol to nuclei of cardiomyocytes. When the failing heart was exposed to stress, the viable myocardium failed to induce Hsp70, suggesting that the failing heart reduces the tolerance against functional damage induced by cardiac stress. It is also found that Hsp60 increases in the failing heart. Since Hsp60 forms protein complex in mitochondria with Hsp10, a molecular shaperon with small molecular weight, Hsp10 content in the failing heart was determined. Although Hsp10 increased in the failing heart, the degree of the increase in Hsp10 in the failing heart was smaller than that in Hsp60. These results suggest that mitochondrial stress is occurred in the failing heart and that imbalance between expressions of Hsp10 and Hsp60 results in a reduction of mitochondrial function in the failing heart following acute myocardial infarction.
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