Uterine Expression of Prostaglandin H2Synthase in Late Pregnancy and during Parturition in Prostaglandin F Receptor-Deficient Mice¹

Dec 30, 1999Endocrinology

Uterus production of prostaglandin-making enzyme late in pregnancy and birth in mice lacking the prostaglandin F receptor

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Abstract

Cyclooxygenase-1 (COX-1) mRNA expression in uterine tissues decreases before parturition but is enhanced in FP-/- mice at term.

Female FP-/- mice cannot deliver normal fetuses at term due to a lack of luteolysis.
COX-1 mRNA is expressed in various uterine tissues throughout late pregnancy in wild-type mice.
A decrease in COX-1 mRNA expression occurs in the endometrial epithelium and myometrium as parturition approaches.
COX-2 mRNA expression is not present in the myometrium before parturition but is significantly induced during parturition.
Induction of COX-2 is absent in FP-/- mice at term but occurs during ovariectomy-induced parturition.
COX-1-derived prostaglandins are likely involved in luteolysis, while COX-2-derived prostaglandins are associated with the final stages of parturition.

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PG production in uterine tissues is important for many physiological processes in late pregnancy, including parturition. We examined the expression of the PGH2 synthases, cyclooxygenase-1 (COX-1) and COX-2, in uterine tissues during late pregnancy, using PGF receptor-deficient (FP-/-) mice. Female FP-/- mice are unable to deliver normal fetuses at term, as they do not undergo luteolysis necessary for parturition. In wild-type mice, COX-1 messenger RNA (mRNA) was expressed in the endometrial epithelium, myometrium, and decidua throughout late pregnancy. The expression of COX-1 mRNA in the endometrial epithelium and myometrium decreased both in wild-type mice undergoing natural parturition and in FP-/- mice undergoing ovariectomy-induced parturition, but expression of COX-1 mRNA was enhanced in FP-/- mice at the expected term. In wild-type mice, COX-2 mRNA was not expressed in the myometrium before parturition, but was markedly induced during parturition. This induction of COX-2 was absent in FP-/- mice at the expected term, but was found during ovariectomy-induced parturition in these mice. Expression of COX-2 proteins was confirmed by immunohistochemical analysis. Thus, in uterine tissues, myometrial expression of COX-2 is closely associated with the occurrence of parturition, but uterine expression of COX-1 is induced much earlier and kept at a high level until parturition occurs. These results suggest that COX-1-derived PGs are responsible for the induction of luteolysis, and that COX-2-derived PGs play a role in the final pathway of parturition.

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Uterine Expression of Prostaglandin H2Synthase in Late Pregnancy and during Parturition in Prostaglandin F Receptor-Deficient Mice¹

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