Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells
Joint Authors
Li, Fang
Cui, Siyuan
Men, Lili
Li, Yu
Zhong, Yingshuo
Yu, Shanshan
Du, Jianling
Source
Issue
Vol. 2018, Issue 2018 (31 Dec. 2018), pp.1-16, 16 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2018-04-01
Country of Publication
Egypt
No. of Pages
16
Main Subjects
Abstract EN
Endothelial dysfunction, partly induced by inflammatory mediators, is known to initiate and promote several cardiovascular diseases.
Selenoprotein S (SelS) has been identified in endothelial cells and is associated with inflammation; however, its function in inflammation-induced endothelial dysfunction has not been described.
We first demonstrated that the upregulation of SelS enhances the levels of nitric oxide and endothelial nitric oxide synthase in tumor necrosis factor- (TNF-) α-treated human umbilical vein endothelial cells (HUVECs).
The levels of TNF-α-induced endothelin-1 and reactive oxygen species are also reduced by the upregulation of SelS.
Furthermore, SelS overexpression blocks the TNF-α-induced adhesion of THP-1 cells to HUVECs and inhibits the increase in intercellular adhesion molecule-1 and vascular cell adhesion molecule-1.
Moreover, SelS overexpression regulates TNF-α-induced inflammatory factors including interleukin-1β, interleukin-6, interleukin-8, and monocyte chemotactic protein-1 and attenuates the TNF-α-induced activation of p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) pathways.
Conversely, the knockdown of SelS with siRNA results in an enhancement of TNF-α-induced injury in HUVECs.
These findings suggest that SelS protects endothelial cells against TNF-α-induced dysfunction by inhibiting the activation of p38 MAPK and NF-κB pathways and implicates it as a possible modulator of vascular inflammatory diseases.
American Psychological Association (APA)
Cui, Siyuan& Men, Lili& Li, Yu& Zhong, Yingshuo& Yu, Shanshan& Li, Fang…[et al.]. 2018. Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells. Mediators of Inflammation،Vol. 2018, no. 2018, pp.1-16.
https://search.emarefa.net/detail/BIM-1203324
Modern Language Association (MLA)
Cui, Siyuan…[et al.]. Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells. Mediators of Inflammation No. 2018 (2018), pp.1-16.
https://search.emarefa.net/detail/BIM-1203324
American Medical Association (AMA)
Cui, Siyuan& Men, Lili& Li, Yu& Zhong, Yingshuo& Yu, Shanshan& Li, Fang…[et al.]. Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells. Mediators of Inflammation. 2018. Vol. 2018, no. 2018, pp.1-16.
https://search.emarefa.net/detail/BIM-1203324
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1203324