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synergistically promote monocyte chemoattractant protein-1 expression: roles of NF-
B, p38, and reactive oxygen species1Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Tokyo; 2Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki; and 3Department of Urology, Faculty of Medicine, and 4Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo, Japan
Submitted 6 December 2007 ; accepted in final form 23 April 2008
We examined whether ANG II and TNF-
cooperatively induce vascular inflammation using the expression of monocyte chemoattractant protein (MCP)-1 as a marker of vascular inflammation. ANG II and TNF- stimulated MCP-1 expression in a synergistic manner in vascular smooth muscle cells. ANG II-induced MCP-1 expression was potently inhibited to a nonstimulated basal level by blockade of the p38-dependent pathway but only partially inhibited by blockade of the NF-
B-dependent pathway. In contrast, TNF--induced MCP-1 expression was potently suppressed by blockade of NF-B activation but only modestly suppressed by blockade of p38 activation. ANG II- and TNF--induced activation of NF-B- and p38-dependent pathways was partially inhibited by pharmacological inhibitors of ROS production. Furthermore, ANG II- and TNF--stimulated MCP-1 expression was partially suppressed by ROS inhibitors. We also examined whether endogenous ANG II and TNF- cooperatively promote vascular inflammation in vivo using a wire injury model of the rat femoral artery. Blockade of both ANG II and TNF- further suppressed neointimal formation, macrophage infiltration, and MCP-1 expression in an additive manner compared with blockade of ANG II or TNF- alone. These results suggested that ANG II and TNF- synergistically stimulate MCP-1 expression via the utilization of distinct intracellular signaling pathways (p38- and NFB-dependent pathways) and that these pathways are activated in ROS-dependent and -independent manners. These results also suggest that ANG II and TNF- cooperatively stimulate vascular inflammation in vivo as well as in vitro.
blood vessels; signaling pathway; atherosclerosis
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