期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 226, 期 6, 页码 1694-1701出版社
WILEY-BLACKWELL
DOI: 10.1002/jcp.22500
关键词
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资金
- National 973 Research Project [2011CB503906]
- National Natural Science Foundation of China for Innovative Research Group [81021001]
- National Natural Science Foundation of China [90813022, 31070735]
- Science and Technology Developmental Project of Shandong Province [2008GG10002014, 2008GG10002034]
Secretion of proinflammatory cytokines by lipopolysaccharide (LPS) activated vascular endothelial cells (VECs) contributes substantially to the pathogenesis of several inflammatory diseases such as atherosclerosis and septic shock. However, the mechanisms involved in this process are not well understood. Here, we investigated the role of phosphatidylcholine-specific phospholipase C (PC-PLC) in LPS-induced IL-8 and MCP-1 production in VECs. The results showed that LPS elevated the level of PC-PLC and the production of IL-8 and MCP-1 in Human umbilical vein vascular endothelial cells (HUVECs). Blocking the function of PC-PLC by exploiting the neutralization antibody of PC-PLC or tricyclodecan-9-yl-xanthogenate (D609), an inhibitor of PC-PLC, significantly inhibited LPS-induced production of IL-8 and MCP-1 in HUVECs. Furthermore, the in vivo experimental results showed that the levels of PC-PLC, IL-8, and MCP-1 in the aortic endothelium and serum were increased in mice injected with LPS. The increased levels of these molecules were also inhibited by the treatment with D609. The data suggested that blocking PC-PLC function significantly inhibited LPS-induced IL-8 and MCP-1 production in cultured HUVECs and in vivo. PC-PLC might be a potential target for therapy in inflammation associated-diseases such as atherosclerosis. J. Cell. Physiol. 226: 1694-1701, 2011. (C) 2010 Wiley-Liss, Inc.
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