In addition, preconditioning MSCs with Ang-II resulted in an increased survival rate and enhanced tube formation via the upregulation of connexin-43 (Cx43), suggesting that priming MSCs with Ang-II improved their therapeutic efficacy by enhancing angiogenesis and gap junction formation, in addition to the paracrine effect of VEGF against MI. This evidence concerns the gene VEGFA and myocardial infarction.