PGE2 release is independent of upregulation of group V phospholipase A2 during long-term stimulation of P388D1 cells with LPS

doi:10.1194/jlr.M500325-JLR200

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A more recent version of this article appeared on November 1, 2005

Papers In Press, published online ahead of print September 8, 2005
J. Lipid Res., doi:10.1194/jlr.M500325-JLR200

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Submitted on July 27, 2005
Revised on August 23, 2005
Accepted on August 26, 2005

PGE₂ release is independent of upregulation of group V phospholipase A₂ during long-term stimulation of P388D₁ cells with LPS

Ursula A Kessen, Ralph H Schaloske, Daren L Stephens, Karin Killermann Lucas, and Edward A. Dennis

Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92037-0601

Corresponding Author: edennis{at}ucsd.edu

P388D1 cells release arachidonic acid and produce prostaglandin E2 (PGE2) upon long-term stimulation with lipopolysaccharide (LPS). The cytosolic Group IVA (GIVA) phospholipase A2 (PLA2) has been implicated in this pathway. LPS stimulation also results in increased expression and secretion of a secretory PLA2, specifically GV PLA2. To test whether GV PLA2 contributes to PGE2-production and whether GIVA PLA2 activation increases the expression of GV PLA2, we utilized the specific GIVA PLA2 inhibitor pyrrophenone and second generation antisense oligonucleotides designed to specifically inhibit expression and activity of GV PLA2. Treatment of P388D1 cells with antisense caused a marked decrease in basal GV PLA2 mRNA and prevented the LPS-induced increase in GV PLA2 mRNA. LPS-stimulated cells release active GV PLA2 into the medium which is inhibited to background levels through antisense treatment. However, LPS-induced PGE2-release by antisense treated cells and by control cells are not significantly different. Collectively, the results suggest that the upregulation of GV PLA2 during long-term LPS-stimulation is not required for PGE2-production by P388D1 cells. Experiments employing pyrrophenone suggested that GIVA PLA2 is the dominant player involved in arachidonic acid release, but it appears not to be involved in the regulation of LPS-induced expression of GV PLA2 or cyclooxygenase-2.

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