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J Biol Chem, Vol. 274, Issue 44, 31245-31248, October 29, 1999
From the Pacific Northwest Research Institute and the Department of
Pharmacology and Medicine, University of Washington,
Seattle, Washington 98122
Interleukin-1
Prostaglandin E2 Mediates Inhibition of Insulin
Secretion by Interleukin-1
(IL-1) and prostaglandin
E2 (PGE2), frequently co-participants in
inflammatory states, are two well recognized inhibitors of
glucose-induced insulin secretion. Previous reports have concluded that
the inhibitory effects of these two autacoids on pancreatic cell
function are not related because indomethacin, a potent prostaglandin
synthesis inhibitor, does not prevent IL-1 effects. However,
indomethacin is not a specific cyclooxygenase inhibitor, and its other
pharmacologic effects are likely to inhibit insulin secretion
independently. Since we recently observed that IL-1 induces
cyclooxygenase-2 (COX-2) gene expression and
PGE2 synthesis in islet cells, we have reassessed the
possibility that PGE2 mediates IL-1 effects on function. By using two cell lines (HIT-T15 and HC13) as well as
Wistar rat isolated pancreatic islets, we examined the ability of two
COX-2-specific antagonists, NS-398 and SC-236, to prevent IL-1
inhibition of insulin secretion. Both drugs prevented IL-1 from
inducing PGE2 synthesis and inhibiting insulin secretion;
adding back exogenous PGE2 re-established inhibition of
insulin secretion in the presence of IL-1. We also found that EP3,
the PGE2 receptor subtype whose post-receptor effect is to decrease adenylyl cyclase activity and, thereby, insulin secretion, is
the dominant mRNA subtype expressed. We conclude that endogenous PGE2 mediates the inhibitory effects of exogenous IL-1
on cell function.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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