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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 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 coincided with the final descent in plasma
progesterone and birth on GD 19.3±0.2.
Implantation of a progesterone-releasing pellet to intact
pregnant dams on GD 16 delayed birth at term until GD
20.9±0.4 and inhibited the GD18 increase in
placental PGF2
levels in conjunction
with a delayed fall in plasma progesterone that reached
its lowest level a day after term birth. The mRNA
abundance levels of uterine activation proteins,
connexin-43 (CX-43), oxytocin receptor (OTR),
PGF2
receptor (FP), and PGHS-2, and the
uterine PGF2
concentrations all
increased at normal term birth. At progesterone-delayed
term birth on GD19.3, even though tissue
PGF2
concentrations were at the high
levels observed at normal term birth, CX-43 and FP mRNA
levels were lower than at normal term birth, thereby
possibly contributing to the delay of birth. These data
are consistent with the concepts 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.
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