Important Role of Angiotensin Receptor Binding Protein in Cardiac Hypertrophy
| Project/Area Number |
21890211
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Yokohama City University |
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Principal Investigator |
SHIGENAGA Atsuichiro Yokohama City University, 附属病院, 助教 (40549903)
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| Co-Investigator(Renkei-kenkyūsha) |
TAMURA Kouichi 横浜市立大学, 医学部, 准教授 (40285143)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥2,522,000 (Direct Cost: ¥1,940,000、Indirect Cost: ¥582,000)
Fiscal Year 2010: ¥1,196,000 (Direct Cost: ¥920,000、Indirect Cost: ¥276,000)
Fiscal Year 2009: ¥1,326,000 (Direct Cost: ¥1,020,000、Indirect Cost: ¥306,000)
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| Keywords | 高血圧学 / 受容体 / 心肥大 / 生体分子 / 高血圧 / トランスレーショナル-リサーチ / トランスレーショナルリサーチ |
|---|
| Research Abstract |
We generated transgenic mice expressing ATRAP specifically in cardiomyocytes under control of the α-myosin heavy chain promoter. In cardiac-specific ATRAP transgenic mice, the development of cardiac hypertrophy, activation of p38 mitogen-activated protein kinase, and expression of hypertrophy-related genes in the context of angiotensin II treatment were completely suppressed, in spite of there being no significant difference in blood pressure on radiotelemetry between the transgenic mice and littermate control mice. These results demonstrate that cardiomyocyte-specific overexpression of ATRAP in vivo abolishes the cardiac hypertrophy provoked by chronic angiotensin II infusion, thereby suggesting ATRAP to be a novel therapeutic target in cardiac hypertrophy.
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Report
(3 results)
Research Products
(19 results)
