APE1/ref1 gene provides anti-oxidative fate to Sca-1 positive cardiac progenitor cells and promotes cardiac repair via macrophage transition in ischemic environment

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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.