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2015 Fiscal Year Final Research Report

The role of ERK5 in diabetic vascular calcification mediated by endothelial-to-mesenchymal transition

Research Project

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Project/Area Number 26860172
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field General pharmacology
Research InstitutionThe University of Tokushima

Principal Investigator

IZAWA-ISHIZAWA Yuki  徳島大学, 大学院医歯薬学研究部, 助教 (40610192)

Project Period (FY) 2014-04-01 – 2016-03-31
Keywords血管石灰化 / 内皮間葉転換 / ERK5 / スタチン
Outline of Final Research Achievements

First of all, we found that pitavastatin, one of lipid lowering agents, can activate ERK5 in endothelial cells by high throughput screening. Pitavastatin increased endothelial nitric oxide synthase (eNOS) expression via ERK5 activation. As eNOS was increased, VE-cadherin, a marker of endothelial cell, was also increased by pitavastatin treatment. NO generation is suggested to regulate VE-cadherin expression and play an important role in the maintain of endothelial cell character. Therefore, it was suggested that pitavastatin might prevent endothelial cells from endothelium-to-mesenchymal transition via ERK5 activation-eNOS expression-NO generation pathway.

Free Research Field

薬理学

URL: 

Published: 2017-05-10  

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