Toll-like receptor 9-stimulated monocyte chemoattractant protein-1 is mediated via JNK-cytosolic phospholipase A2-ROS signaling

被引：47

作者：

Lee, Jin-Gu ^{[1
]}

Lee, Sun-Hye ^{[1
]}

Park, Dae-Weon ^{[1
]}

Lee, Sang-Hoon ^{[1
]}

Yoon, Hong-Sik ^{[1
]}

Chin, Byung-Ro ^{[1
]}

Kim, Jung-Hye ^{[1
]}

Kim, Jae-Ryong ^{[1
]}

Baek, Suk-Hwan ^{[1
]}

机构：

[1] Yeungnam Univ, Coll Med, Dept Biochem & Mol Biol, Aging Associted Vasc Dis Res Ctr,Dept Dent, Taegu 705717, South Korea

来源：

CELLULAR SIGNALLING | 2008年 / 20卷 / 01期

关键词：

lipopolysaccharide; CpG; toll-like receptor; cPL A(2); MCP-1;

D O I：

10.1016/j.cellsig.2007.09.003

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Monocyte chemoattractant protein-1 (MCP-1) influences monocyte migration into sites of inflammation. This study highlights the importance of cytosolic phospholipase A(2) (cPLA(2))-mediated reactive oxygen species (ROS) signaling processes in the regulation of MCP-1 release as a result of toll-like receptor (TLR) activation. In macrophages, activation of TLR9 induced MCP-1 and cPLA(2)-phosphotylated arachidonic acid (AA) release. Inhibition of cPLA(2) blocked CpG-induced MCP-1 and AA release. Although CpG stimulates phosphorylation of ERK, p38 and JNK, only inhibition of the JNK signaling pathways attenuated MCP-1 release, suggesting that the TLR9-mediated MCP-1 release was dependent upon the JNK pathway. TLR9 activation also stimulated ROS generation, while inhibition of NADPH oxidases (Noxs) blocked CpG-induced MCP-1 release. The CpG treatment increased macrophage Nox1 mRNA level, however it had no effect on macrophage Nox2 mRNA level. Overall, these results suggest that CpG enhances ROS generation through cPLA(2)-dependent pathways, which results in MCP-1 release. (C) 2007 Elsevier Inc. All rights reserved.

引用

页码：105 / 111

页数：7

共 31 条

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