Secreted frizzled-related protein 5 protects against oxidative stress-induced apoptosis in human aortic endothelial cells via downregulation of Bax

被引：11

作者：

Wang, Xiaojie ^{[1
]}

Peng, Qing ^{[2
]}

Jiang, Feng ^{[2
]}

Xue, Li ^{[2
]}

Li, Jiafu ^{[2
]}

Fan, Zhongcai ^{[2
]}

Chen, Pan ^{[1
]}

Chen, Guo ^{[1
]}

Cai, Yihua ^{[2
]}

机构：

[1] Southwest Med Univ, Affiliated Hosp, Dept Endocrinol, Luzhou, Peoples R China

[2] Southwest Med Univ, Affiliated Hosp, Dept Cardiol, Luzhou, Peoples R China

来源：

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY | 2017年 / 31卷 / 12期

关键词：

apoptosis; atherosclerosis; endothelial cells; oxidative stress; SFRP5; MITOCHONDRIAL DYSFUNCTION; SFRP5; EXPRESSION; ANGIOTENSIN-II; IN-VIVO; PATHWAY; CANCER; INJURY; ATHEROSCLEROSIS; CARDIOMYOCYTES; PROLIFERATION;

D O I：

10.1002/jbt.21978

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

This study was undertaken to determine the role of secreted frizzled-related protein 5 (SFRP5) in endothelial oxidative injury. Human aortic endothelial cells (HAECs) were exposed to different oxidative stimuli and examined for SFRP5 expression. The effects of SFRP5 overexpression and knockdown on cell viability, apoptosis, and reactive oxygen species production were measured. HAECs treated with angiotensin (Ang) II (1M) or oxidized low-density lipoprotein (oxLDL) (150g/mL) showed a significant increase in SFRP5 expression. Overexpression of SFRP5 significantly attenuated the viability suppression and apoptosis induction by Ang II and oxLDL, whereas the knockdown of SFRP5 exerted opposite effects. Overexpression of SFRP5 prevented ROS formation and -catenin activation and reduced Bax expression. Co-expression of Bax significantly reversed the anti-apoptotic effect of SFRP5 overexpression, whereas knockdown of Bax restrained Ang II- and oxLDL-induced apoptosis in HAECs. Taken together, SFRP5 confers protection against oxidative stress-induced apoptosis through inhibition of -catenin activation and downregulation of Bax.

引用

页数：6

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