Prostaglandin-Endoperoxide Synthase 1 Mediates the Timing of Parturition in Mice Despite Unhindered Uterine Contractility

Oct 14, 2017Endocrinology

An enzyme controls the timing of birth in mice even when the uterus can contract normally

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Abstract

Delayed parturition in Cox-1 knockout mice is associated with impaired luteolysis and cervical dilation.

Cox-1 knockout mice did not show differences in embryo implantation or postimplantation growth.
Messenger RNAs of contraction-associated proteins were expressed differently in Cox-1 knockout compared to wild-type myometrium.
There were no differences in intracellular calcium release or uterine contractility between Cox-1 knockout and wild-type mice.
Delayed parturition persisted in Cox-1 knockout mice even with exogenous oxytocin treatment.
Withdrawal of progesterone improved the delayed parturition phenotype in Cox-1 knockout mice.
Cox-1 knockout mice exhibited decreased cervical distensibility on the expected delivery day.

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Cyclooxygenase (COX)-derived prostaglandins stimulate uterine contractions and prepare the cervix for parturition. Prior reports suggest Cox-1 knockout (KO) mice exhibit delayed parturition due to impaired luteolysis, yet the mechanism for late-onset delivery remains unclear. Here, we examined key factors for normal onset of parturition to determine whether any could account for the delayed parturition phenotype. Pregnant Cox-1KO mice did not display altered timing of embryo implantation or postimplantation growth. Although messenger RNAs of contraction-associated proteins (CAPs) were differentially expressed between Cox-1KO and wild-type (WT) myometrium, there were no differences in CAP agonist-induced intracellular calcium release, spontaneous or oxytocin (OT)-induced ex vivo uterine contractility, or in vivo uterine contractile pressure. Delayed parturition in Cox-1KO mice persisted despite exogenous OT treatment. Progesterone (P4) withdrawal, by ovariectomy or administration of the P4-antagonist RU486, diminished the delayed parturition phenotype of Cox-1KO mice. Because antepartum P4 levels do not decline in Cox-1KO females, P4-treated WT mice were examined for the effect of this hormone on in vivo uterine contractility and ex vivo cervical dilation. P4-treated WT mice had delayed parturition but normal uterine contractility. Cervical distensibility was decreased in Cox-1KO mice on the day of expected delivery and reduced in WT mice with long-term P4 treatment. Collectively, these findings show that delayed parturition in Cox-1KO mice is the result of impaired luteolysis and cervical dilation, despite the presence of strong uterine contractions.

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Prostaglandin-Endoperoxide Synthase 1 Mediates the Timing of Parturition in Mice Despite Unhindered Uterine Contractility

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