Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells.
Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells.
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硒蛋白 S 可减轻肿瘤坏死因子-α 诱导的内皮细胞功能障碍。
DOI：
10.1155/2018/1625414
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发表时间：
2018
影响因子：
4.6
通讯作者：
Du J
中科院分区：
文献类型：
--
作者：
Cui S;Men L;Li Y;Zhong Y;Yu S;Li F;Du J
内皮功能障碍，部分由炎症介质引起，是已知的启动和促进几种心血管疾病。硒蛋白S（SelS）已被确定在内皮细胞中，并与炎症有关，然而，其在炎症诱导的内皮功能障碍尚未被描述。我们首次证实了SelS的上调可增强肿瘤坏死因子-（TNF-）α处理的人脐静脉内皮细胞（HUVECs）中一氧化氮和内皮型一氧化氮合酶的水平。TNF-α诱导的内皮素-1和活性氧水平也因SelS的上调而降低。此外，SelS过表达可阻断TNF-α诱导的THP-1细胞与HUVECs的粘附，并抑制细胞间粘附分子-1和血管细胞粘附分子-1的表达。此外，SelS过表达调节TNF-α诱导的炎症因子，包括白细胞介素-1 β、白细胞介素-6、白细胞介素-8和单核细胞趋化蛋白-1，并减弱TNF-α诱导的p38丝裂原活化蛋白激酶（MAPK）和核因子-κB（NF-κB）通路的激活。相反，用siRNA敲低SelS导致TNF-α诱导的HUVECs损伤增强。这些结果表明SelS通过抑制p38 MAPK和NF-κB通路的激活来保护内皮细胞免受TNF-α诱导的功能障碍，并暗示它可能是血管炎性疾病的调节剂。
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.
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DOI：
10.1042/cs20080196
发表时间：
2009-02
期刊：
Clinical science (London, England : 1979)
影响因子：
--
作者：
Zhang H;Park Y;Wu J;Chen Xp;Lee S;Yang J;Dellsperger KC;Zhang C
通讯作者：
Zhang C
影响因子：
7.7
作者：
Gao, Y;Walder, K;Collier, GR
通讯作者：
Collier, GR
人 β-防御素 3 减少 TNF-α 诱导的人脐静脉内皮细胞炎症和单核细胞粘附
影响因子：
4.6
作者：
Bian T;Li H;Zhou Q;Ni C;Zhang Y;Yan F
通讯作者：
Yan F
DOI：
10.1165/rcmb.2013-0187oc
发表时间：
2014-06-01
影响因子：
6.4
作者：
Sun, Xutong;Kumar, Sanjiv;Black, Stephen M.
通讯作者：
Black, Stephen M.
影响因子：
64.8
作者：
Ye, YH;Shibata, Y;Rapoport, TA
通讯作者：
Rapoport, TA