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A more recent version of this article appeared on April 1, 2006

Papers In Press, published online ahead of print December 28, 2005
J. Lipid Res., doi:10.1194/jlr.M500369-JLR200
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Submitted on August 15, 2005
Revised on December 9, 2005
Accepted on December 27, 2005

Involvement of cAMP response element-binding protein-1 in arachidonic acid-induced vascular smooth muscle cell motility

Nagadhara Dronadula, Farhan Rizvi, Eva Blaskova, Quanyi Li, and Gadiparthi N. Rao

Physiology Dept., University of Tennessee Health Science Center, Memphis, TN 38163

Corresponding Author: grao{at}physio1.utmem.edu

Arachidonic acid and its eicosanoid metabolites in addition to their role in many vital cellular functions are involved in the pathogenesis of several diseases including atherosclerosis and cancer. To understand the potential mechanisms by which these lipid molecules could influence the disease processes, particularly cardiovascular diseases, here we have studied arachidonic acid effects on vascular smooth muscle cell (VSMC) motility and the role of cyclic AMP-response element binding protein-1 (CREB-1) in this process. Arachidonic acid (AA) exerted differential effects on VSMC motility; at lower doses it stimulated motility while at higher doses it was inhibitory. AA-induced VSMC motility requires its conversion via the LOX and COX pathways. AA stimulated the phosphorylation of ERKs, JNKs and p38MAPK in a time-dependent manner and blockade of these serine/threonine kinases significantly attenuated AA-induced VSMC motility. In addition, AA stimulated CREB-1 phosphorylation and activity in a manner that is also dependent on its metabolic conversion via the LOX and COX pathways and activation of ERKs and p38MAPK but not JNKs. Furthermore, suppression of CREB-1 activation inhibited AA-induced VSMC motility. 15(S)-HETE and PGF2a, the 15-LOX and COX metabolites of arachidonic acid, respectively, that are produced by VSMC, at lower doses were also found to stimulate motility in these cells. Together, these results suggest that AA induces VSMC motility by complex mechanisms involving its metabolism via the LOX and COX pathways as well as ERK- and p38MAPK-dependent and JNK-independent activation of CREB-1.


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