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Regular Article |
a Department of Molecular and Integrative Physiology, Ralph L. Smith Research Center, University of Kansas Medical Center, Kansas City, Kansas 66160-7338
b The DuPont Pharmaceuticals Co., Wilmington, Delaware 19880-0400
c Department of Medicine (Nephrology) and Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2372
ABSTRACT
Previous observations of ovulation and fertilization defects in cyclooxygenase-2 (COX-2)-deficient mice suggested that COX-2-derived ovarian prostaglandins (PGs) participate in these events. However, the specific PG and its mode of action were unknown. Subsequent studies revealed that mice deficient in EP2, a PGE2-receptor subtype, have reduced litter size, apparently resulting from poor ovulation but more dramatically from impaired fertilization. Using a superovulation regimen and in vitro culture system, we demonstrate herein that the ovulatory process, not follicular growth, oocyte maturation, or fertilization, is primarily affected in adult COX-2- or EP2-deficient mice. Furthermore, our results show that in vitro-matured and -fertilized eggs are capable of subsequent preimplantation development. However, severely compromised ovulation in adult COX-2- or EP2-deficient mice is not manifested in immature (3-wk-old) COX-2- or EP2-deficient mice, suggesting that the process of ovulation is more dependent on PGs in adult mice. Although the processes of implantation and decidualization are defective in COX-2(-/-) mice, our present results demonstrate that these events are normal in EP2-deficient mice, as determined by embryo transfer and experimentally induced decidualization. Collectively, previous and present results suggest that whereas COX-2-derived PGE2 is essential for ovulation via activation of EP2, COX-2-derived prostacyclin is involved in implantation and decidualization via activation of peroxisome proliferator-activated receptor
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First decision: 5 December 2000.
1 Supported in part by a grant from the Mellon Foundation, NICHD grants HD 12304 and HD 29968, as part of the National Cooperative Program on Markers of Uterine Receptivity for Blastocyst Implantation (S.K.D.), and NIGMS grant GM 15431 (R.M.B.). S.K.D. is an NICHD (NIH) MERIT Awardee. H.M. is a KUMC Biomedical postdoctoral fellow. Center grants in Reproductive Biology (HD 33994) and Mental Retardation (HD 02528) from the NIH provided access to various core facilities.
2 Correspondence: Sudhansu K. Dey, Department of Molecular and Integrative Physiology, MRRC 37/3017, University of Kansas Medical Center, Kansas City, KS 66160-7338. FAX: 913 588 5677; sdey{at}kumc.edu
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