Long non-coding RNA H19 contributes to hypoxia-induced CPC injury by suppressing Sirt1 through miR-200a-3p.

Cardiomyocyte death is the chief obstacle that prevents the heart function recovery in myocardial infarction (MI)-induced heart failure (HF). Cardiac progenitor cells (CPCs)-based myocardial regeneration has provided a promising method for heart function recovery after MI. However, CPCs can easily lose their proliferation ability due to oxygen deficiency in infarcted myocardium. Revealing the underlying molecular mechanism for CPC proliferation is critical for effective MI therapy. In the present study, we set up a CoCl2-induced hypoxia model in CPCs. We found that the expression of long non-coding RNA H19 was significantly down-regulated in CPCs after hypoxia stimuli. In addition, H19 suppression attenuated the proliferation and migration of CPCs under hypoxia stress. Furthermore, we discovered that H19 regulated the proliferation and migration of CPCs through mediating the expression of Sirt1 which is a target of miR-200a-3p under hypoxia. In conclusion, our findings demonstrate a novel regulatory mechanism for the proliferation and migration of CPCs under hypoxia condition, which provides useful information for the development of new therapeutic targets for MI therapy.