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Vol. 13, No. 12, pp. 1561-1574, June 15, 1999
1 Department of Molecular and Integrative Physiology,
University of Kansas Medical Center, Kansas City, Kansas 66160-7338 USA; 2 Department of Gastroenterology/Medicine,
Vanderbilt University, Nashville, Tennessee 37232-2279 USA;
3 Merck Research Laboratories, Rahway, New Jersey 07065 USA;
4 Department of Medicine and Pharmacology, Vanderbilt
University, Nashville, Tennessee 37232-6602 USA; 5 The DuPont
Pharmaceuticals Company, Wilmington, Delaware 19880 USA
We have demonstrated previously that cyclo-oxygenase-2 (COX2), the
rate-limiting enzyme in the biosynthesis of prostaglandins (PGs), is
essential for blastocyst implantation and decidualization. However, the
candidate PG(s) that participates in these processes and the mechanism
of its action remain undefined. Using COX2-deficient mice and
multiple approaches, we demonstrate herein that COX2-derived prostacyclin (PGI2) is the primary PG that is essential for
implantation and decidualization. Several lines of evidence suggest
that the effects of PGI2 are mediated by its activation of
the nuclear hormone receptor PPAR
, demonstrating the first reported
biologic function of this receptor signaling pathway.
[Key Words:
COX2; prostaglandins; PPAR; mouse; implantation]
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