Loss of cyclooxygenase-2 retards decidual growth but does not inhibit embryo implantation or development to term.
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.
Cheng
Jr-Gang
JG
Cancer and Developmental Biology Laboratory, National Cancer Institute at Frederick, Frederick, Maryland 21702, USA.
Stewart
Colin L
CL
D000818:Animals; D002452:Cell Count; D051546:Cyclooxygenase 2; D003656:Decidua / Q000254:growth & development*; D010064:Embryo Implantation; D005314:Embryonic and Fetal Development; D005260:Female; D005306:Fertilization; D006579:Heterozygote; D007527:Isoenzymes / Q000172:deficiency / Q000502:physiology*; D008297:Male; D051379:Mice; D009865:Oocytes / Q000473:pathology; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000378:metabolism / Q000502:physiology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000172:deficiency / Q000502:physiology*; D011555:Pseudopregnancy / Q000503:physiopathology; D013997:Time Factors; D014886:Weaning
D007527:Isoenzymes; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases