MicroRNA‑126 and VEGF enhance the function of endothelial progenitor cells in acute myocardial infarction

Abstract

Previous studies have found that microRNA‑126 (miR‑126) overexpression can exert beneficial effects on endothelial function and angiogenesis. The role of miR‑126 was previously reported to be by directly limiting the activities of negative regulators of the vascular endothelial growth factor (VEGF) pathway, such as PI3K regulation subunit 2 (PIK3R2). The aim of the present study was to investigate the role of the miR‑126/PIK3R2/VEGF axis in endothelial progenitor cells (EPCs) under hypoxic conditions. An in vitro hypoxia model in EPCs was established by exposing EPCs to hypoxia (O2/N2/CO2, 1/94/5) for 72 h, before reverse transcription‑quantitative PCR (RT‑qPCR) and western blot analyzes were used to measure miR‑126 and PIK3R2 expression in EPCs. The proliferation, migration and tube‑forming ability of the transfected cells were measured using MTT, Transwell and tube formation assays, respectively. miR‑126 expression was found to be lower in EPCs in the hypoxia group compared with that in the control group (P<0.01). The expression of PIK3R2, a direct target gene of miR‑126, was found to be higher in the hypoxia group compared with that in the control group (P<0.01). miR‑126 mimic and VEGF‑plasmid co‑transfection improved the proliferation, migration, tube‑forming ability and restored the phosphorylation of AKT in EPCs under hypoxic conditions (all P<0.01). In addition, the effects of miR‑126 mimic on hypoxia‑induced EPCs were reversed by PIK3R2‑plasmid co‑transfection, whilst the effects of VEGF‑plasmid were enhanced further by co‑transfection with the miR‑126 mimic. In conclusion, miR‑126 promoted the functions of EPCs under hypoxic conditions by negatively targeting PIK3R2, whilst the combined overexpression of miR‑126 and VEGF enhanced these aforementioned effects.