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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Dusting, G. J. Jiang, F. Guo, N. |
| Description | Author Affiliation: Jiang F ( Bernard O'Brien Institute of Microsurgery, University of Melbourne, Victoria, Australia. fjiang@unimelb.edu.au) |
| Abstract | BACKGROUND AND PURPOSE: We investigated the effects of a synthetic flavonol, 3',4'-dihydroxyflavonol (DiOHF) on the expression of monocyte chemoattractant protein-1 (MCP-1) in rat vascular smooth muscle cells. EXPERIMENTAL APPROACH: MCP-1 expression was assessed by quantitative real-time PCR and protein phosphorylation by immunoprecipitation and Western blots. KEY RESULTS: DiOHF (1-30 micromol x L(-1)) concentration-dependently reduced MCP-1 expression in both quiescent cells and cells stimulated with platelet-derived growth factor (PDGF) or interleukin 1-beta. The effect of DiOHF was associated with a suppression of focal adhesion kinase (FAK)-mediated signalling. In vitro kinase assays demonstrated that DiOHF is a potent inhibitor of FAK kinase activity (EC(50)= 2.4 micromol x L(-1)). Expression of FAK-related non-kinase reduced basal MCP-1 expression, but not that induced by PDGF or interleukin 1-beta. DiOHF also inhibited autophosphorylation of PDGF receptors. The PDGF receptor inhibitor AG-1296 potently suppressed basal and PDGF-induced MCP-1 expression. Inhibition of extracellular signal-regulated kinase activation by DiOHF, either directly or indirectly, may also be involved in its effects on MCP-1 expression. DiOHF had no inhibitory effect on either p38 or nuclear factor-kappaB activation. Moreover, DiOHF inhibited smooth muscle cell spreading (a FAK-mediated response) and proliferation. CONCLUSIONS AND IMPLICATIONS: This is the first report on a flavonoid compound (DiOHF) that is a potent FAK inhibitor. DiOHF also inhibits PDGF receptor autophosphorylation. These effects underlie the inhibitory action of DiOHF on MCP-1 expression in smooth muscle cells. Our results suggest that DiOHF might be a useful tool for dissection of the (patho)physiological roles of FAK signalling. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 4 |
| Volume Number | 157 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 2009-06-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Chemokine CCL2 Biosynthesis Down-Regulation Drug Effects Flavonols Pharmacology Focal Adhesion Protein-Tyrosine Kinases Antagonists & Inhibitors Muscle, Smooth, Vascular Animals Cell Movement Cell Proliferation Cells, Cultured Cytokines Physiology Mitogen-Activated Protein Kinase 1 Metabolism NF-kappa B Phosphorylation Protein-Tyrosine Kinases Rats, Sprague-Dawley Receptors, Platelet-Derived Growth Factor P38 Mitogen-Activated Protein Kinases Research Support, Non-U.S. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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