Induction of heme oxygenase 1 by arsenite inhibits cytokine-induced monocyte adhesion to human endothelial cells

被引:14
作者
Sun, Xi [1 ]
Pi, Jingbo [2 ]
Liu, Wenlan [1 ]
Hudson, Laurie G. [1 ]
Liu, Ke Jian [1 ]
Feng, Changjian [1 ]
机构
[1] Univ New Mexico 1, Coll Pharm, Albuquerque, NM 87131 USA
[2] Hamner Inst Hlth Sci, Div Translat Biol, Res Triangle Pk, NC 27709 USA
关键词
Arsenic; Endothelial cells; Heme oxygenase 1; Cytokine; Monocyte adhesion; NF-KAPPA-B; GENE-EXPRESSION; CARDIOVASCULAR-DISEASE; DRINKING-WATER; CHEMOATTRACTANT PROTEIN-1; VASCULAR-DISEASE; OXIDATIVE STRESS; IN-VITRO; EXPOSURE; ATHEROSCLEROSIS;
D O I
10.1016/j.taap.2009.01.023
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Heme oxygenase-1 (HO-1) is an oxidative stress responsive gene upregulated by various physiological and exogenous stimuli. Arsenite, as an oxidative stressor, is a potent inducer of HO-1 in human and rodent cells. In this study, we investigated the mechanistic role of arsenite-induced HO-1 in modulating tumor necrosis Factor alpha (TNF-alpha) induced monocyte adhesion to human umbilical vein endothelial cells (HUVEC). Arsenite pretreatment, which upregulated HO-1 in a time and concentration-dependent manner, inhibited TNF-alpha-induced monocyte adhesion to HUVEC and intercellular adhesion molecule 1 protein expression by 50% and 40%, respectively importantly, knockdown of HO-1 by small interfering RNA abolished the arsenite-induced inhibitory effects. These results indicate that induction of HO-1 by arsenite inhibits the cytokine-induced monocyte adhesion to HUVEC by suppressing adhesion molecule expression. These Findings established in important mechanistic link between the functional monocyte adhesion properties of HUVEC and the induction of HO-1 by arsenite. (C) 2009 Elsevier Inc. All rights reserved
引用
收藏
页码:202 / 209
页数:8
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