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J Biol Chem, Vol. 274, Issue 37, 25967-25970, September 10, 1999
From the Department of Chemistry and Biochemistry, University of
California at San Diego, La Jolla, California 92093-0601
When exposed for prolonged periods of
time (up to 20 h) to bacterial lipopolysaccharide (LPS) murine
P388D1 macrophages exhibit a delayed prostaglandin
biosynthetic response that is entirely mediated by cyclooxygenase-2
(COX-2). Both the constitutive Group IV cytosolic phospholipase
A2 (cPLA2) and the inducible Group V secretory
phospholipase A2 (sPLA2) are involved in the
cyclooxygenase-2-dependent generation of prostaglandins in
response to LPS. Using the selective sPLA2 inhibitor
3-(3-acetamide-1-benzyl-2-ethylindolyl-5-oxy)propane sulfonic acid
(LY311727) and an antisense oligonucleotide specific for Group V
sPLA2, we found that induction of COX-2 expression is
strikingly dependent on Group V sPLA2, which was further
confirmed by experiments in which exogenous Group V sPLA2
was added to the cells. Exogenous Group V sPLA2 was able to
induce significant arachidonate mobilization on its own and to induce
expression of the COX-2. None of these effects was observed if inactive
Group V sPLA2 was utilized, implying that enzyme activity
is crucial for these effects to take place. Therefore, not only delayed
prostaglandin production but also COX-2 gene
induction are dependent on a catalytically active Group V
sPLA2. COX-2 expression was also found to be blunted by the
Group IV cPLA2 inhibitor methyl arachidonyl
fluorophosphonate, which we have previously found to block Group V
sPLA2 induction as well. Collectively, the results support
a model whereby Group IV cPLA2 activation regulates the
expression of Group V sPLA2, which in turn is responsible
for delayed prostaglandin production by regulating COX-2 expression.
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