2014 Fiscal Year Final Research Report
Suppression of Cardiovascular Remodeling by Base Excision Repair of Oxidative DNA Damage and Heat Shock Protein
Project/Area Number |
24591031
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
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Research Institution | Asahikawa Medical College |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2015-03-31
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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.
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Free Research Field |
循環器病学
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