MiRNA-26a promotes angiogenesis in a rat model of cerebral infarction via PI3K/AKT and MAPK/ERK pathway.

Abstract

To investigate the specific role of microRNA-26 (miRNA-26a) in a rat model of cerebral ischemic stroke and the underlying mechanism. A rat model of middle cerebral artery occlusion (MCAO) was established to induce permanent cerebral infarction. Neuro-behavior was observed and scored after model establishment. The expression of miRNA-26a in brain tissue and brain microvascular endothelial cells (BMECs) of rats after cerebral ischemic stroke was detected by quantitative polymerase chain reaction (qPCR). The formation of the endothelial lumen was detected by Matrigel assay after BMECs were transfected with miR-26a mimics or inhibitors. Besides, cell proliferation after miRNA-26a transfection was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. The protein levels related to PI3K/AKT and MAPK/ERK signaling pathway were detected by Western blot. miRNA-26a expression was elevated after cerebral infarction injury. Further investigation showed that miRNA-26a mimics could promote endothelial lumen formation and cell proliferation in BMECs, while miRNA-26a inhibitor inhibited the capacity of lumen formation and cell proliferation. Notably, we found that miRNA-26a might up-regulate the expression of HIF-1a via activating the AKT and ERK1/2 pathway, thus mediating the transcriptional activity of VEGF and promoting lumen formation and cell proliferation in BMECs. MiRNA-26a promotes angiogenesis in a rat model of cerebral ischemic via PI3K/AKT and MAPK/ERK pathway.