NR6A1 promotes vascular smooth muscle cell apoptosis by up-regulating RIPK3 gene expression

VernacularTitle:核受体NR6A1通过上调RIPK3基因表达诱导血管平滑肌细胞凋亡
Author: hui Ya ZHANG ¹ ; Xiong WANG ; ying Sheng WU ; xia Ji PENG ; yun Fu WU ; Jing KE ; Peng ZHANG ; fang Qiu ZHANG ; xia Yan LV
Author Information

1. 湖北医药学院病理生理学教研室
Keywords: Nuclear receptor subfamily 6,group A,member 1; Receptor-interacting serine/threonine-protein kinase 3; Apoptosis
From: Chinese Journal of Pathophysiology 2017;33(9):1581-1586
CountryChina
Language:Chinese
Abstract: AIM:To determine the role of nuclear receptor subfamily 6,group A,member 1 (NR6A1) in vascular smooth muscle cell (VSMC) apoptosis.METHODS:NR6A1 protein was over-expressed in the VSMCs by infection of adenovirus.The effect of NR6A1 on the viability of VSMCs was measured by MTT assay.DAPI staining,TUNEL staining and caspase activity assay were conducted.DNA microarray was used to quickly screen the target genes of NR6A1.The effect of receptor-interacting serine/threonine-protein kinase 3 (RIPK3) silencing on NR6A1-induced apoptosis of the VSMCs was further analyzed.RESULTS:Adenovirus-mediated over-expression of NR6A1 induced the apoptosis of VSMCs.The RIPK3 gene expression was up-regulated by NR6A1 over-expression in the VSMCs.NR6A1-induced VSMC apoptosis was inhibited by RIPK3 silencing.CONCLUSION:NR6A1 promotes VSMC apoptosis by up-regulating the RIPK3 gene expression.