2013 Fiscal Year Final Research Report
APE1/ref1 gene provides anti-oxidative fate to Sca-1 positive cardiac progenitor cells and promotes cardiac repair via macrophage transition in ischemic environment
| Project/Area Number |
23618002
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Regenerative medicine
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KAWABE Jun-ichi 旭川医科大学, 医学部, 特任准教授 (10400087)
HASEBE Naoyuki 旭川医科大学, 医学部, 教授 (30192272)
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUBARA Hiroaki (10239072)
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| Project Period (FY) |
2011 – 2013
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| Keywords | Ape1 / 心筋再生 / 抗炎症 |
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| Research Abstract |
The ROS production and apoptosis stimulated by H2O2 were significantly reduced in Ape1-CPCs compared with DsRed-CPCs. At 4 weeks, the absolute change in the LVEF was significantly greater in Ape1-CPCs injected mouse, but not DsRed-CPCs, than in the placebo group, that was associated with reduced infarcted size. Ape1-CPCs injected mouse were significantly enhanced the engraft cells compared with DsRed-CPCs injected mouse. In infarct myocardium of Ape1-CPCs injected mouse, M1 macrophages, but not M2 macrophages, were significantly reduced compared with that of DsRed-CPCs injected mouse. APE1/ref1 gene enhances the survival of engraft Sca1-CPC accompanied with the redox effect against oxidative stress in ischemic myocardium. Great survived Sca1-CPCs repaired the loss of LV function, which were associated with reduced infarcted myocardium and inflammation via macrophage transition. These results may provide an APE1/ref1 gene as a novel target to innovate the cardiac cell-therapy.
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