Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells
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 dysfunct...
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2018/1625414 |
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| author | Siyuan Cui Lili Men Yu Li Yingshuo Zhong Shanshan Yu Fang Li Jianling Du |
| author_facet | Siyuan Cui Lili Men Yu Li Yingshuo Zhong Shanshan Yu Fang Li Jianling Du |
| author_sort | Siyuan Cui |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-c3fcc46291404b49b72b37976d313caf |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-c3fcc46291404b49b72b37976d313caf2025-02-03T01:03:29ZengWileyMediators of Inflammation0962-93511466-18612018-01-01201810.1155/2018/16254141625414Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial CellsSiyuan Cui0Lili Men1Yu Li2Yingshuo Zhong3Shanshan Yu4Fang Li5Jianling Du6Department of Endocrinology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, ChinaDepartment of Endocrinology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, ChinaDepartment of Endocrinology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, ChinaDepartment of Endocrinology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, ChinaDepartment of Endocrinology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, ChinaDepartment of Immunology, Dalian Medical University, Dalian, Liaoning 116044, ChinaDepartment of Endocrinology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, ChinaEndothelial 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.http://dx.doi.org/10.1155/2018/1625414 |
| spellingShingle | Siyuan Cui Lili Men Yu Li Yingshuo Zhong Shanshan Yu Fang Li Jianling Du Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells Mediators of Inflammation |
| title | Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells |
| title_full | Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells |
| title_fullStr | Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells |
| title_full_unstemmed | Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells |
| title_short | Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells |
| title_sort | selenoprotein s attenuates tumor necrosis factor α induced dysfunction in endothelial cells |
| url | http://dx.doi.org/10.1155/2018/1625414 |
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