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Inhibitory effect of thrombin on the expression of secretory group IIA phospholipase A 2
Author(s) -
Bae JongSup
Publication year - 2011
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.23172
Subject(s) - thrombin , umbilical vein , lipopolysaccharide , phospholipase c , phospholipase a2 , ly294002 , chemistry , microbiology and biotechnology , receptor , kinase , pharmacology , enzyme , biochemistry , biology , phosphatidylinositol , endocrinology , immunology , platelet , in vitro
It is well known that the expression level of secretory group IIA phospholipase A 2 (sPLA 2 ‐IIA) is elevated in inflammatory diseases and lipopolysaccharide (LPS) up‐regulates the expression of sPLA 2 ‐IIA in human umbilical vein endothelial cells (HUVECs). Recently, lower concentration thrombin could elicit anti‐inflammatory responses in HUVECs. Here, the effects of lower concentration thrombin on the expression of sPLA 2 ‐IIA in LPS‐stimulated HUVECs were investigated. Prior treatment of cells with thrombin (25–75 pM) inhibited LPS‐induced sPLA 2 ‐IIA expression by activating its receptor, protease‐activated receptor‐1 (PAR‐1). And pretreatment of cells with either PI3‐kinase inhibitor (LY294002) or cholesterol depleting agent (methyl‐β‐cyclodextrin, MβCD) abolished the inhibitory activity of thrombin against sPLA 2 ‐IIA expression. Therefore, these results suggest that PAR‐1 activation by lower concentration thrombin inhibited LPS mediated expression of sPLA 2 ‐IIA by PAR‐1 and PI3‐kinase‐dependent manner in lipid raft on the HUVECs. J. Cell. Biochem. 112: 2502–2507, 2011. © 2011 Wiley‐Liss, Inc.