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Objectives   MicroRNA-125b (miR-125b) has been recognized as one of the key regulators of the inflammatory responses in cardiovascular diseases recently. This study sought to dissect the role of miR-125b in modulating the function of endothelial progenitor cells (EPCs) in the inflammatory environment of ischemic hearts.Methods   EPCs were cultured and transfected with miR-125b mimic and negative control mimic. Cell migration and adhesion assays were performed after tumor necrosis factor- α  (TNF- α ) treatment to determine EPC function. Cell apoptosis was analyzed by flow cytometry. The activation of the NF- κ B pathway was measured by western blotting. EPC-mediated neovascularization in vivo was studied by using a myocardial infarction model.Results   miR-125b-overexpressed EPCs displayed improved cell migration, adhesion abilities, and reduced cell apoptosis compared with those of the NC group after TNF- α  treatment. miR-125b overexpression in EPCs ameliorated TNF- α -induced activation of the NF- κ B pathway. Mice transplanted with miR-125b-overexpressed EPCs showed improved cardiac function recovery and capillary vessel density than the ones transplanted with NC EPCs.Conclusions   miR-125b protects EPCs against TNF- α -induced inflammation and cell apoptosis by attenuating the activation of NF- κ B pathway and consequently improves the cardiac function recovery and EPC-mediated neovascularization in the ischemic hearts.

Upregulation of MicroRNA-125b Leads to the Resistance to Inflammatory Injury in Endothelial Progenitor Cells