Deficiency of peroxisome proliferator-activated receptor α attenuates apoptosis and promotes migration of vascular smooth muscle cells.

• 发表时间: Sep 2021
• 来源期刊: Biochem Biophys Rep
• DOI: 10.1016/j.bbrep.2021.101091
• PMID: 34381883
• 文章类型: Journal Article
• 作者列表: Duan Y,Qi D,Liu Y,Song Y,Wang X,Jiao S,Li H,Gonzalez FJ,Qi Y,Xu Q,Du J,Qu A

关键词: Ang II, angiotensin II; Angiotensin II; EC, endothelial cell; ECM, extracellular matrix; ERK, extracellular signal-regulated kinase; MAPK, mitogen-activated protein kinase; MCP-1, monocyte chemoattractant protein-1; PCR, polymerase chain reaction; PPAR, peroxisome proliferator-activated receptor; PPARα; SM22α, smooth muscle 22α; TGF, tumor growth factor; TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling; VSMC, vascular smooth muscle cell; Vascular remodeling; Vascular smooth muscle cell

Abstract

Peroxisome proliferator-activated receptor (PPAR) α is widely expressed in the vasculature and has pleiotropic and lipid-lowering independent effects, but its role in the growth and function of vascular smooth muscle cells (VSMCs) during vascular pathophysiology is still unclear. Herein, VSMC-specific PPARα-deficient mice (Ppara ΔSMC) were generated by Cre-LoxP site-specific recombinase technology and VSMCs were isolated from mice aorta. PPARα deficiency attenuated VSMC apoptosis induced by angiotensin (Ang) II and hydrogen peroxide, and increased the migration of Ang II-challenged cells.