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This version published online on June 5, 2003
Endocrinology, doi:10.1210/en.2003-0420
A more recent version of this article appeared on August 1, 2003
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*PROSTAGLANDIN F2ALPHA

Submitted on April 4, 2003
Accepted on May 27, 2003

Prostaglandin F2{alpha} and Prolactin Signaling: PGF2{alpha}-mediated Inhibition of Prolactin Receptor Expression in the Corpus Luteum

Carlos Stocco1, Jean Djiane1, and and Geula Gibori1*

1 Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, IL, 60612, Unite' de Biologie Cellulaire et Mole'culaire, Institut National de la Recherche Agronomique (INRA), 78352 Jouy-en-Josas Cedex, France.

* To whom correspondence should be addressed. E-mail: ggibori{at}uic.edu.

It is well established that prolactin (PRL) sustains, while prostaglandin F2{alpha} (PGF2{alpha}) curtails, progesterone production by the rodent corpus luteum (CL). We have previously shown that PGF2{alpha} inhibits the expression of several luteal genes stimulated by PRL, while stimulating other genes inhibited by this hormone. We have also found that PGF2{alpha} stimulation of 20{alpha}hydroxysteroid dehydrogenase (20{alpha}HSD), 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{alpha} and to also find out whether PGF2{alpha} opposes PRL action by inhibiting PRL-R expression. Using the PGF2{alpha} receptor (PGF2{alpha}-R) knockout, we examined whether the absence of the PGF2{alpha}-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, where both forms of the PRL-R decline to low levels between days 18-20 of pregnancy, expression of these receptors remained elevated in the PGF2{alpha}-R null mice. Furthermore, administration of PGF2{alpha} to pregnant rats inhibited PRL-R expression. Time course analysis revealed that PGF2{alpha} treatment decreases both isoforms of PRL-R within 1 h of treatment in vivo whereas its stimulatory effect on 20{alpha}HSD expression was further delayed. Similar results were obtained with luteinized granulosa cell in culture. To examine whether the decline in PRL-R is involved/necessary for PGF2{alpha} action, cells were transfected with a constitutively active PRL-R (PRL-Rca). The expression of this receptor did not prevent PGF2{alpha} effect on PRL-R or 20{alpha}HSD expression. Taken together, these results demonstrate that PGF2{alpha} 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{alpha}. The results further suggest that PGF2{alpha}-mediated stimulation of 20{alpha}HSD is independent from PGF2{alpha} inhibition of PRL signaling in luteal cell.




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