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J. Biol. Chem., Vol. 279, Issue 29, 30579-30587, July 16, 2004

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Prostaglandin E₂ Is a Product of Induced Prostaglandin-endoperoxide Synthase 2 and Microsomal-type Prostaglandin E Synthase at the Implantation Site of the Hamster^*

Xiaohong Wang, Yan Su, Kaushik Deb, Monika Raposo, Jason D. Morrow¶||, Jeff Reese, and Bibhash C. Paria**

From the Division of Reproductive and Developmental Biology, the Department of Pediatrics, the ^¶Department of Medicine and Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2678 and University of Kansas Medical Center, Kansas City, Kansas 66160-7338

Certain uterine prostaglandins (PGs) are elevated at implantation sites and are needed to trigger the events of blastocyst implantation that include blastocyst-uterine attachment and stromal decidualization with vascular permeability changes. Several decades of investigations showed that treatment with PG synthesis inhibitors, prior to or during the time of implantation, resulted in either complete inhibition or a delay in implantation or reduction in the number of implantation sites with diminished decidual tissue. Consistent with these findings, we observed that whereas a selective PG endoperoxide synthase (Ptgs) 1 inhibitor SC-560 failed to inhibit implantation, a selective Ptgs2 inhibitor SC-236 showed significantly reduced number and size of implantation sites in progesterone-treated ovariectomized pregnant hamsters. It is known that Ptgs2 expression and Ptgs2-derived prostacyclin (PGI₂) synthesis at implantation sites are needed for implantation in the mouse (a rodent that needs ovarian estrogen for implantation). However, it is unknown which Ptgs and PG synthases produce which PGs at implantation sites of the hamster (a rodent that does not need ovarian estrogen for implantation). Here we demonstrate that as blastocyst implantation proceeds, a reduction in Ptgs1 expression from uterine luminal epithelial cells and a gradual induction in Ptgs2 expression exclusively in luminal epithelial and adjacent decidual cells occurred at implantation sites of hamsters. Results also reveal that PGE₂, but not PGI₂, is the major PG at implantation sites where Ptgs2 and microsomal type PGE synthases but not PGI synthases are co-expressed. This elevated uterine PGE₂ at implantation sites may serve to initiate or amplify physiological signals required for specific aspects of the implantation process in hamsters.

Received for publication, January 20, 2004 , and in revised form, March 26, 2004.

^* This work was supported in part by National Institutes of Health Grants HD 42636, HD 44741, HD 40193, HD 37394 (to B. C. P.), GM 15431, CA 77839, DK 48831, RR 00095 (to J. D. M.), and HD 40221 (to J. R.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^|| Recipient of a Burroughs Wellcome Fund Clinical Scientist Award in Translational Research.

^** To whom correspondence should be addressed: Division of Reproductive and Developmental Biology, Dept. of Pediatrics, Vanderbilt University Medical Center, 1161 21st Ave. South, Nashville, TN 37232-2678. Tel.: 615-322-8640; Fax: 915-322-4704; E-mail: bc.paria{at}vanderbilt.edu.

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