MiR-17-5p promotes the endothelialization of endothelial progenitor cells to facilitate the vascular repair of aneurysm by regulating PTEN-mediated PI3K/AKT/VEGFA pathway

Abstract

ABSTRACT The endothelialization of endothelial progenitor cells (EPCs) was proven to facilitate the vascular repair of aneurysm. MiR-17-5p regulated angiogenesis in various cancers. This research focused on exploring the effect of miR-17-5p on EPCs and the vascular repair of aneurysm. In vivo study: the aneurysm rat model was established and treated with AgomiR-17-5p; the histopathology of aneurysm tissues was examined by hematoxylin-eosin staining; and the level of EPCs in the aneurysm tissues and peripheral blood of rats were evaluated by immunofluorescence and flow cytometry, respectively. In vitro study: EPCs were cultured and identified using flow cytometry; the target of miR-17-5p was proven by dual-luciferase reporter assay; after transfection, the viability, migration, and tube formation of the EPCs were detected by MTT, wound healing, and tube formation assays, respectively; the expressions of VEGFA and factors related to PTEN-mediated PI3K/AKT pathway were detected by ELISA, qPCR, or Western blot as needed. In vivo study: miR-17-5p overexpression promoted the vascular repair in aneurysm rats and increased the level of EPCs in the aneurysm tissues and peripheral blood of the rats. In vitro study: miR-17-5p overexpression promoted the viability, migration, and tube formation of EPCs, up-regulated the expressions of VEGFA, p-PI3K, and p-AKT, and down-regulated the PTEN expression in EPCs; miR-17-5p silencing did the opposite; PTEN was targeted by miR-17-3p and further abrogated the effects of miR-17-5p overexpression on EPCs. MiR-17-5p promoted the endothelialization of EPCs to facilitate the vascular repair of aneurysm by regulating PTEN-mediated PI3K/AKT/VEGFA pathway.