Omentin inhibits TNF-α-induced expression of adhesion molecules in endothelial cells via ERK/NF-κB pathway

被引:158
作者
Zhong, Xia [1 ]
Li, Xiaonan [1 ]
Liu, Fuli [1 ]
Tan, Hui [1 ]
Shang, Deya [1 ]
机构
[1] Shandong Univ, Prov Hosp, Dept Emergency, Jinan 250021, Peoples R China
关键词
Omentin; ERK; NF-kappa B; ICAM-1; VCAM-1; TYPE-2; DIABETES-MELLITUS; CORONARY ATHEROSCLEROSIS; METABOLIC DISEASE; INFLAMMATION; ACTIVATION; ADIPOKINES; TRANSCRIPTION; ASSOCIATION;
D O I
10.1016/j.bbrc.2012.07.110
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In the present study, we investigated whether omentin affected the expression of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in tumor necrosis factor-alpha (TNF-alpha) induced human umbilical vein endothelial cells (HUVECs). Our data showed that omentin decreased TNF-alpha-induced expression of ICAM-1 and VCAM-1 in HUVECs. In addition, omentin inhibited TNF-alpha-induced adhesion of THP-1 cells to HUVECs. Further, we found that omentin inhibited TNF-alpha-activated signal pathway of nuclear factor-kappa B (NF-kappa B) by preventing NF-kappa B inhibitory protein (I kappa B alpha) degradation and NF-kappa B/DNA binding activity. Omentin pretreatment significantly inhibited TNF-alpha-induced ERR activity and ERR phosphorylation in HUVECs. Pretreatment with PD98059 suppressed TNF-alpha-induced NF-kappa B activity. Omentin, NF-kB inhibitor (BAY11-7082) and ERR inhibitor (PD98059) reduced the up-regulation of ICAM-1 and VCAM-1 induced by TNF-alpha. These results suggest that omentin may inhibit TNF-alpha-induced expression of adhesion molecules in endothelial cells via blocking ERK/NF-kappa B pathway. (c) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:401 / 406
页数:6
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