Exploration of epigenome abnormalities involved in salt sensitive hypertension

2015 Fiscal Year Final Research Report

• Project/Area Number: 26670426
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Kidney internal medicine
• Research Institution: The University of Tokyo
• 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)
• 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)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: エピゲノム / 食塩感受性高血圧 / DNAメチル化

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.

Free Research Field

腎臓内分泌内科