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A more recent version of this article appeared on March 1, 2003

Papers In Press, published online ahead of print January 1, 2003
J. Lipid Res., doi:10.1194/jlr.M200092-JLR200
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Submitted on February 26, 2002
Revised on December 19, 2002
Accepted on December 20, 2002

Different effects of n-6 and n-3 polyunsaturated fatty acids on the activation of rat smooth muscle cells by interleukin-1beta

Souad Bousserouel, Arthur Brouillet, Gilbert Bereziat, Michel Raymondjean, and Marise Andreani

UMR 7079 Physiologie et Physiopathologie, Université Pierre et Marie Curie (Paris6), Paris, Cedex 5 75252

Corresponding Author: arthur.brouillet{at}snv.jussieu.fr

There is good evidence that the n-3 polyunsaturated fatty acids (PUFA) in fish-oil have anti-inflammatory effects and reduce the pathogenesis of atherosclerosis. However, the mechanisms underlying these actions are largely unknown. This study was designed to investigate the effects of membrane incorporation of two major components of fish-oil (EPA and DHA), on rat smooth muscle cells (SMC) activation induced by interleukin-1beta (IL1beta ). We compared their effects with those of n-6 arachidonic acid (AA). Expression of VCAM-1 and MCP-1 adhesion molecules involved in SMC migration, was enhanced by AA, whereas EPA and DHA had no similar effects. We established that AA potentiates IL1beta -induced expression of the type IIA secretory phospholipase A2 (sPLA2) gene, whereas EPA and DHA reduce this stimulation. EPA and DHA also abolished pro-inflammatory prostaglandin PGE2 production by inhibiting the IL1beta -induced production of cyclooxygenase COX-2 mRNA. Then much interest was focused on three transcriptional factors implicated in inflammation control and especially in modulating rat sPLA2 and COX-2 gene transcription : NF-KB, C/EBP beta and Ets-1. EMSA revealed that the binding activity of all three factors was increased by AA and reduced (or not affected) by n-3 PUFA. These results indicate that EPA and DHA act in opposition to AA by modulating various steps of the inflammatory process induced by IL1beta , probably by reducing MAP kinase p42/p44 activity.


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