Effects of selenoprotein S on oxidative injury in human endothelial cells

Journal of Translational Medicine

Research

Li-li Men¹  Hai-cheng Zhou¹  Qian Xing¹  Yin Zhao¹  Chun-hong Shi¹  Jian-ling Du¹  Jun-jie Yao¹  Rong-chong Huang¹  Hua Li² 

[1] Department of Endocrinology, The First Affiliated Hospital of Dalian Medical University, 116011, Dalian, Liaoning, China;Department of Pharmacology, College of Pharmacy, Dalian Medical University, 116044, Dalian, Liaoning, China;

关键词: Endothelial cell dysfunction;    Oxidation;    Selenoprotein S;    Caveolin-1;    Protein kinase Cα;   

DOI  :  10.1186/1479-5876-11-287

 received in 2013-06-06, accepted in 2013-10-30,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundSelenoprotein S (SelS) is an important endoplasmic reticulum and plasma membrane-located selenoprotein implicated in inflammatory responses and insulin resistance. However, the effects of SelS on endothelial cells (ECs) have not been reported. In the present study, the role of SelS in oxidative stress and the underlying mechanism were investigated in human ECs.MethodsA SelS over-expression plasmid (pc-SelS) and a SelS-siRNA plasmid were transfected into human umbilical vein endothelial cells (American Type Culture Collection, USA). The cells were divided into four groups: control, SelS over-expression (transfected with pc-SelS), vector control, and SelS knockdown (transfected with siRNA-SelS). After treating the cells with H2O2, the effects of oxidative stress and the expression of caveolin-1 (Cav-1) and protein kinase Cα (PKCα) were investigated.ResultsFollowing treatment with H2O2, over-expression of SelS significantly increased cell viability and superoxide dismutase (SOD) activity, and decreased malondialdehyde (MDA) production and Cav-1 gene and protein expression. However, no effects on PKCα were observed. In contrast, knockdown of SelS significantly decreased cell viability, SOD activity, and PKCα gene and protein expression, and increased MDA production and Cav-1 gene and protein expression.ConclusionsSelS protects ECs from oxidative stress by inhibiting the expression of Cav-1 and PKCα.

【 授权许可】

Unknown   
© Zhao et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.