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Mouse Placental Prostaglandins Are Associated with Uterine Activation and the Timing of Birth¹

^a The Perinatal Research Centre, CIHR Group in Perinatal Health and Disease, Departments of Obstetrics and Gynaecology, Pediatrics, and Physiology, University of Alberta, Edmonton, Alberta, Canada T6G 2S2

We explored a potential mechanism linking placental prostaglandins (PGs) with a fall in plasma progesterone and increased expression of uterine activation proteins in the mouse. PG endoperoxide H synthase 2 (PGHS-2) mRNA expression increased in placenta in late gestation in association with an 8-fold increase in PGF₂ concentration, reaching a peak on Gestational Day (GD) 18. This peak coincided with the final descent in plasma progesterone and birth on GD 19.3 ± 0.2. Implantation of a progesterone-releasing pellet in intact pregnant dams on GD 16 delayed birth at term until GD 20.9 ± 0.4 and inhibited the GD 18 increase in placental PGF₂ levels in conjunction with a delayed fall in plasma progesterone that reached its lowest level 1 day after term birth. The mRNA levels of uterine activation proteins, connexin-43 (CX-43), oxytocin receptor, PGF₂ receptor (FP), and PGHS-2, and the concentration of uterine PGF₂ all increased at normal term birth. At progesterone-delayed term birth on GD 19.3, even though tissue PGF₂ concentrations were at the same high levels observed at normal term birth, CX-43 and FP mRNA levels were lower than those at normal term birth, thereby possibly contributing to the delay of birth. These data are consistent with the hypotheses that fetal placental PGs affect the timing of birth by hastening luteolysis, that uterine activation initiates labor, and that birth may be delayed by blocking or decreasing the expression of two of the uterine activation proteins.

¹ This research was supported by the Alberta Heritage Foundation for Medical Research, the Canadian Institutes of Health Research, the National Science and Engineering Research Council, the University of Alberta Perinatal Research Centre, and the University of Alberta Faculty of Medicine.

² Correspondence: David M. Olson, Perinatal Research Centre, 220 HMRC, University of Alberta, Edmonton, AB, Canada T6G 2S2. FAX: 780 492 1308; david.olson{at}ualberta.ca

³ Current address: Health Canada, Ottawa, ON, Canada

⁴ Joint first authors

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