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

Abstract EN

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-κB 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-κB 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-κB pathway and consequently improves the cardiac function recovery and EPC-mediated neovascularization in the ischemic hearts.