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Prostaglandin F₂ (PGF₂) and Prolactin Signaling: PGF₂-Mediated Inhibition of Prolactin Receptor Expression in the Corpus Luteum

Department of Physiology and Biophysics (C.S., G.G.), University of Illinois at Chicago, Chicago, Illinois 60612; and Unité de Biologie Cellulaire et Moléculaire (J.D.), Institut National de la Recherche Agronomique, 78352 Jouy-en-Josas Cedex, France

Address all correspondence and requests for reprints to: Geula Gibori, Department of Physiology and Biophysics (M/C 901), University of Illinois, 835 South Wolcott Avenue, Chicago, Illinois 60612. E-mail: ggibori{at}uic.edu.

Abstract

It is well established that prolactin (PRL) sustains, whereas prostaglandin F₂ (PGF₂) curtails, progesterone production by the rodent corpus luteum (CL). We have previously shown that PGF₂ inhibits the expression of several luteal genes stimulated by PRL, whereas it stimulates other genes inhibited by this hormone. We have also found that PGF₂ stimulation of 20-hydroxysteroid dehydrogenase (20HSD), an enzyme that catabolizes progesterone, at the end of pregnancy is accompanied by a dramatic decrease in PRL receptor (PRL-R) expression. These findings, and the fact that the factors that inhibit PRL-R are not known, led us to examine in vivo whether the decline in PRL-R at the end of pregnancy is due to PGF₂ and to also find out whether PGF₂ opposes PRL action by inhibiting PRL-R expression. Using the PGF₂ receptor (PGF₂-R) knockout, we examined whether the absence of the PGF₂-R prevents the decline in the expression of both the short and long forms of the PRL-R in the CL. We found that, in sharp contrast to the wild-type mice, in which both forms of the PRL-R decline to low levels between d 18–20 of pregnancy, expression of these receptors remained elevated in the PGF₂-R null mice. Furthermore, administration of PGF₂ to pregnant rats inhibited PRL-R expression. Time-course analysis revealed that PGF₂ treatment decreases both isoforms of PRL-R within 1 h of treatment in vivo, whereas its stimulatory effect on 20HSD expression was further delayed. Similar results were obtained with luteinized granulosa cells in culture. To examine whether the decline in PRL-R is involved/necessary for PGF₂ action, cells were transfected with a constitutively active PRL-R. The expression of this receptor did not prevent PGF₂ effect on PRL-R or 20HSD expression. Taken together, these results demonstrate that PGF₂ inhibits the expression of the PRL-R and that the decline in both forms of the PRL-R that occurs at the end of pregnancy in the CL is due to PGF₂. The results further suggest that PGF₂-mediated stimulation of 20HSD is independent from PGF₂ inhibition of PRL signaling in luteal cell.

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