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Journal of Lipid Research, Vol. 44, 601-611, March 2003
Copyright © 2003 by Lipid Research, Inc.

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

Souad Bousserouel, Arthur Brouillet¹, Gilbert Béréziat, Michel Raymondjean and Marise Andréani

^me UMR Physiologie et Physiopathologie, Université Pierre et Marie Curie, case courrier 256, Bâtiment A, 5, étage, 7 quai Saint Bernard, 75252 Paris Cedex 5, France

¹ To whom correspondence should be addressed. e-mail: arthur.brouillet{at}snv.jussieu.fr

There is good evidence that the n-3 polyunsaturated fatty acids (PUFAs) in fish oil have antiinflammatory 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 [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)], on rat smooth muscle cells (SMCs) activation induced by interleukin-1ß (IL1ß). We compared their effects with those of n-6 arachidonic acid (AA). Expression of vascular cell adhesion molecule-1 and monocyte chemoattractant protein-1 adhesion molecules involved in SMCs migration was enhanced by AA, whereas EPA and DHA had no similar effects. We established that AA potentiates IL1ß-induced expression of the type IIA secreted phospholipase A2 (sPLA2) gene, whereas EPA and DHA reduce this stimulation. EPA and DHA also abolished proinflammatory prostaglandin PGE2 production by inhibiting the IL1ß-induced production of cyclooxygenase-2 (COX-2) mRNA. Much interest was then focused on three transcriptional factors implicated in inflammation control and especially in modulating rat sPLA2 and COX-2 gene transcription: nuclear factor-B, CCAAT/enhancer binding protein ß, and E26 transformation-specific-1. electrophoretic mobility shift assay 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 IL1ß, probably by reducing mitogen-activated protein kinase p42/p44 activity.

Abbreviations: AA, arachidonic acid; C/EBP, CCAAT/enhancer binding protein; COX-2, cyclooxygenase-2; DHA, docosahexaenoic acid; EMSA, electrophoretic mobility shift assay; EPA, eicosapentaenoic acid; ERK, extracellular signal-regulated kinase; IL1ß, interleukin-1ß; MAPK, mitogen-activated protein kinase; MCP-1, monocyte chemoattractant protein-1; MEK, MAPK kinase; SMC, smooth muscle cell; sPLA2, secreted phospholipase A2; VCAM-1, vascular cell adhesion molecule-1; ZAL, Z-IE(o-t-butyl)A-leucinal

Supplementary key words eicosapentaenoic acid • docosahexaenoic acid • type IIA secretory phospholipase A2

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