Publication Date:
2017-12-06
Description:
Cerebral ischemic stroke (CIS) is one of the common causes of death and disability worldwide. This study aims to investigate effect of miR-137 on endothelial progenitor cells and angiogenesis in CIS by targeting NR4A2 via the Notch pathway. Brain tissues were extracted from CIS and normal mice. Immunohistochemistry was used to determine positive rate of NR4A2 expression. Serum VEGF, Ang, HGF and IκBα levels were determined by ELISA. RT-qPCR and western blotting were used to determine expression of related factors. Endothelial progenitor cells in CIS mice were treated and grouped into blank, NC, miR-137 mimics, miR-137 inhibitors, siRNA-NR4A2 and miR-137 inhibitors + siRNA-NR4A2 groups, and cells in normal mice into normal group. Proliferation and apoptosis were determined by MTT and flow cytometry, respectively. NR4A2 protein expression was strongly positive in CIS mice, which showed higher serum levels of VEGF, Ang and HGF but lower IκBα than normal mice. Compared with normal group, the rest groups (endothelial progenitor cells from CIS mice) showed decreased expressions of miR-137, Hes1, Hes5 and IκBα but elevated NR4A2, Notch, Jagged1, Hey-2, VEGF, Ang and HGF, inhibited proliferation and enhanced apoptosis. Compared with blank and NC groups, the miR-137 mimics and siRNA-NR4A2 groups exhibited increased expression of miR-137, Hes1, Hes5 and IκBα, but decreased NR4A2, Notch, Jagged1 and Hey-2, with enhanced proliferation and attenuated apoptosis. The miR-137 inhibitors group reversed the conditions. miR-137 enhances the endothelial progenitor cell proliferation and angiogenesis in CIS mice by targeting NR4A2 through the Notch signaling pathway. This article is protected by copyright. All rights reserved
Electronic ISSN:
1097-4652
Topics:
Biology
,
Medicine
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