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Experimental & Molecular Medicine ; : 757-764, 2009.
Article in English | WPRIM | ID: wpr-71507

ABSTRACT

Monocyte chemoattractant protein-1 (MCP1) plays a key role in monocyte/macrophage infiltration to the sub-endothelial space of the blood vessel wall, which is a critical initial step in atherosclerosis. In this study, we examined the intracellular signaling pathway of IL-1beta-induced MCP1 expression using various chemical inhibitors. The pretreatment of a phosphatidylcholine (PC)-specific PLC (PC-PLC) inhibitor (D609), PKC inhibitors, or an NF-kappaB inhibitor completely suppressed the IL-1beta-induced MCP1 expression through blocking NF-kappaB translocation to the nucleus. Pretreatment with inhibitors of tyrosine kinase or PLD partially suppressed MCP1 expression and failed to block nuclear NF-kappaB translocation. These results suggest that IL-1beta induces MCP1 expression through activation of NF-kappaB via the PC-PLC/PKC signaling pathway.


Subject(s)
Humans , Active Transport, Cell Nucleus/drug effects , Aorta/pathology , Atherosclerosis/immunology , Bridged-Ring Compounds/pharmacology , Cell Nucleus/metabolism , Cells, Cultured , Chemokine CCL2/biosynthesis , Estrenes/pharmacology , Genistein/pharmacology , Interleukin-1beta/metabolism , Myocytes, Smooth Muscle/drug effects , NF-kappa B/metabolism , Phospholipases/antagonists & inhibitors , Protein-Tyrosine Kinases/antagonists & inhibitors , Pyrrolidinones/pharmacology , Recombinant Proteins/metabolism , Signal Transduction/drug effects , Thiones/pharmacology
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