Loss of cyclooxygenase-2 retards decidual growth but does not inhibit embryo implantation or development to term |
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Authors: | Cheng Jr-Gang Stewart Colin L |
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Affiliation: | Cancer and Developmental Biology Laboratory, National Cancer Institute at Frederick, Frederick, Maryland 21702, USA. |
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Abstract: | 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. |
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