MiR-130a-3p inhibits endothelial inflammation by regulating the expression of MAPK8 in endothelial cells

Abstract

MicroRNA-130a-3p (miR-130a-3p) has been reported as closely related to atherosclerosis (AS). This study is to survey the effects of miR-130a-3p in endothelial cells (ECs) treated with oxidized low-density lipoprotein (ox-LDL) and explore underlying mechanisms. The proliferation and apoptosis of ox-LDL-treated HUVEC cells were determined by CCK-8, EdU, and flow cytometry assays. ELISA and Western blot analysis measured the expressions of cytokines and protein levels. Bioinformatics and dual-luciferase reporter assay were performed to predict and confirm that Mitogen-activated protein kinase 8 (MAPK8) was a direct target of miR-130a-3p, and MAPK8 was negatively associated with miR-130a-3p. As expected, miR-130a-3p was down-regulated in ox-LDL-treated HUVEC cells, and up-regulation of miR-130a-3p promoted proliferation and inhibited apoptosis of ox-LDL-treated HUVEC cells. Furthermore, miR-130a-3p mimics suppressed the expressions of TNF-α and IL-6 and decreased the protein levels of VCAM-1, ICAM-1 and E-selectin. MAPK8 was highly expressed in ox-LDL-treated HUVEC cells, and silence of MAPK8 promoted proliferation inhibited apoptosis, suppressed inflammatory responses, and decreased the levels of VCAM-1, ICAM-1, and E-selectin, over-expression of MAPK8 partially restored the functional effects of miR-130a-3p on proliferation, inflammatory responses, and the expressions of VCAM-1, ICAM-1 and E-selectin. This study indicates that miR-130a-3p may emerge as an effective target for treating AS.