| Project/Area Number |
26670426
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Kidney internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Fujita Toshiro 東京大学, 先端科学技術研究センター, 特任研究員、名誉教授 (10114125)
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| Co-Investigator(Kenkyū-buntansha) |
MARUMO Takeshi 東京大学, 先端科学技術研究センター 臨床エピジェネティクス講座, 特任准教授 (70265817)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | エピゲノム / 食塩感受性高血圧 / DNAメチル化 / エピジェネティクス / 高血圧 / 腎臓 |
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| Outline of Final Research Achievements |
Aberrant epigenome may underlie the pathogenesis of salt sensitive hypertension. We analyzed changes in molecules involved in salt reabsorption in a cell-type specific manner. We found that the promoter region of angiotensinogen is aberrantly demethylated in the proximal tubules of diabetic mice, which develop hypertension (J Am Soc Nephrol 2015). Aberrant demethylation of angiotensinogen may lead to persistent activation of salt absorption and/or renal injury.
In addition, we observed that pendrin, a molecule involved in reabsorption of salt, is upregulated in hypertension induced by infusion of angiotensin II. We collected intercalated cells from Atp6v1b1-EGFP mice by sorting and now investigating the changes in epigenome.
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