| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| 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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