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BOR - Papers in Press, published online ahead of print October 17, 2002.
Biol Reprod 2002, 10.1095/biolreprod.102.009589
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BIOLOGY OF REPRODUCTION 68, 401–404 (2003)
DOI: 10.1095/biolreprod.102.009589
© 2003 by the Society for the Study of Reproduction, Inc.

Female Reproductive Tract

Loss of Cyclooxygenase-2 Retards Decidual Growth but Does Not Inhibit Embryo Implantation or Development to Term

Jr-Gang Chenga, and Colin L. Stewart1,a

a Cancer and Developmental Biology Laboratory, National Cancer Institute at Frederick, Frederick, Maryland 21702

Previous reports have described that female mice deficient in cyclooxygenase-2 (COX2) are largely infertile because of failure to ovulate, poor fertilization, and defective implantation and decidualization. In the present study, we reinvestigated reproduction in these mice and found they do show a reduction in the numbers of ovulated and fertilized eggs. However, we did not observe any substantial effect on embryo implantation frequencies or an inability of COX2-deficient females to support embryo development to weaning. Pseudopregnant COX2-null recipients do not show any alteration in the timing of implantation following blastocyst transfer, but they do show a delay in the initial rate of decidual growth after implantation that lags by approximately 24 h compared to that in heterozygous or wild-type recipients. These results support previous findings that COX2 has a role in mediating the initial uterine decidual response but is not essential to sustaining decidual growth and embryo development throughout the remainder of pregnancy.

1 Correspondence. FAX: 301 846 7117; stewartc{at}ncifcrf.gov




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