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2014 Fiscal Year Final Research Report

Suppression of Cardiovascular Remodeling by Base Excision Repair of Oxidative DNA Damage and Heat Shock Protein

Research Project

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Project/Area Number 24591031
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Circulatory organs internal medicine
Research InstitutionAsahikawa Medical College

Principal Investigator

HASEBE Naoyuki  旭川医科大学, 医学部, 教授 (30192272)

Project Period (FY) 2012-04-01 – 2015-03-31
Keywords酸化ストレス / 心血管リモデリング / DNA塩基損傷 / APE1 / 内皮前駆細胞
Outline of Final Research Achievements

The aim of this study was to establish a new strategy for control of cardiovascular remodeling through the base excision repair of oxidative DNA damage and heat shock protein. The main target protein was Apurinic/apyrimidinic Endonuclease 1 (APE1). The adhesion property of endothelial progenitor cells (EPCs) was maintained depending on APE1 activity. The neo-intimal formation in the wire-injured femoral arteries of mice, i.e. intima/media ratio was significantly suppressed by APE1. Heat shock protein 72 was expressed mainly in the media of APE1-applied wire-injured lesion, accompanied by suppression of chemocaines and NADPH oxidase, suggesting the suppression of inflamation and oxidative stress. We proposed a potential new strategy of modifying APE1 mediated mechanism for the suppression of cardiovascular remodeling.

Free Research Field

循環器病学

URL: 

Published: 2016-06-03  

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