Effects of selenoprotein S on oxidative injury in human endothelial cells

Journal of Translational Medicine

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

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

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

Others  :  1234489
DOI  :  10.1186/1479-5876-11-287

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

【 摘 要 】

Background

Selenoprotein 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.

Methods

A 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.

Results

Following 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.

Conclusions

SelS protects ECs from oxidative stress by inhibiting the expression of Cav-1 and PKCα.

【 授权许可】

   
2013 Zhao et al.; licensee BioMed Central Ltd.

【 图 表 】

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