| Project/Area Number |
24591595
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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 |
Pediatrics
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| Research Institution | National Cardiovascular Center Research Institute |
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Principal Investigator |
SHIRAI Manabu 独立行政法人国立循環器病研究センター, 研究所, 室長 (70294121)
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| Co-Investigator(Renkei-kenkyūsha) |
MORISKI Takayuki 国立循環器病研究センター, 研究所, 部長 (30174410)
MORISKI Hiroko 国立循環器病研究センター, 研究所, 室長 (40311451)
HONDA Takehiko 国立循環器病研究センター, 研究所, 室員 (10455545)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | ポリコーム遺伝子群 / 心臓発生 / 心不全 / ポリコーム遺伝子 / 心臓形態形成 / 発生医学 |
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| Outline of Final Research Achievements |
To understand whether the Polycomb group (PcG) protein, Pcgf5, is implicated in maintaining balance between self-renewal and differentiation of cardiac progenitor cells, we generated Pcgf5 deficient mice. Homozygous mice were smaller than wild type. They were, however, fertile, and did not show any obvious developmental abnormalities. At around 1 year old, only homozygotes died with cardiac dysfunction. Pcgf5 deficient cardiomyocytes were hypertrophic and disorganized, however, no significant difference of cell proliferation and death between controls and homozygotes. Since 6 months old, Pcgf5 deficient males showed decrease of left ventricular ejection fraction, enlargement of the heart and upregulation of expression of Nppa/ANP, Acta1/αSK and Myh7/βMhc, known to be upregulated by cardiac overloading. These findings indicate that Pcgf5 plays a pivotal role in maintaining the cardiac function in aged mice.
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