| Project/Area Number |
21790889
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Endocrinology
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | アルドステロン / エピジェネティクス / DNAメチル化 / 組織特異的プロモーター / CYP11B2 / 核内受容体 / 心筋症 / 心肥大 / 肥大型心筋症 |
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| Research Abstract |
In addition to the primary effect of aldosterone to induce sodium and fluid retention, excess aldosterone has direct inflammatory and fibrotic effects contributing to target organ deterioration, leading to the development of vascular, renal, and cardiac inflammation ; fibrosis ; and hypertrophy. Although the adrenal gland is a major source of aldosterone, aldosterone production and levels of mRNA coding for CYP11B2 are induced in the ventricles during hypertrophy, and aldosterone synthesis from heart itself causes cardiac hypertrophy. We showed a role for DNA methylation in CYP11B2 gene repression and suggest an epigenomic mechanism may be causally linked with an increase in cardiac aldosterone production in the pathophysiology of the heart. Meanwhile, nuclear receptors(NGFIB, NURR1, NOR1, SF1) involved in aldosteronogenesis differentially employed multiple alternative promoters(APs) in a tissue-specific manner. The use of APs was different between human adrenal and cardiovascular tissues.
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