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J. Biol. Chem., Vol. 275, Issue 47, 37202-37211, November 24, 2000
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From the Prostaglandin F2
Prostaglandin F2
-induced Expression of
20-Hydroxysteroid Dehydrogenase Involves the Transcription Factor
NUR77*
,,
Department of Physiology and Biophysics,
University of Illinois College of Medicine, Chicago, Illinois 60612, the § Department of Physiological Chemistry, Faculty of
Pharmaceutical Sciences, Kyoto University, Kyoto 606-8501, Japan,
and the ¶ Department of Molecular Genetics, University of Illinois
College of Medicine, Chicago, Illinois 60612
(PGF2) binding to its receptor on the rat corpus luteum
triggers various signal transduction pathways that lead to the
activation of a steroidogenic enzyme, 20-hydroxysteroid dehydrogenase (20-HSD), which in turn catabolizes progesterone. The
molecular mechanism underlying PGF2-induced 20-HSD
enzyme activity has not yet been explored. In this report we show,
using mice lacking PGF2 receptor and pregnant rats, that
PGF2 is responsible for the rapid and massive expression
of the 20-HSD gene at the end of pregnancy leading to a decrease in
progesterone secretion. We also present evidence that
PGF2 enhances 20-HSD promoter activity. We have
determined a region upstream of the 
1590 position in the 20-HSD
promoter that confers regulation by PGF2 in ovarian primary cells. This region encompasses a unique transcription factor-binding site with a sequence of a NUR77 response element. Deletion of this motif or overexpression of a NUR77 dominant negative protein caused a complete loss of 20-HSD promoter activation by
PGF2. NUR77 also transactivated the 20-HSD promoter
in transient transfection experiments in corpus luteum-derived cells
(GG-CL). This induction required the NUR77-transactivating domain. We
also show that PGF2 induces a very rapid expression of
NUR77 that binds to a distal response element located at 1599/1606
but does not interact with another proximal putative NUR77 response element located downstream in the promoter. A rapid increase in NUR77
mRNA was observed in mice corpora lutea just before parturition at
a time when 20-HSD becomes expressed. This increase in the expression of both genes was not seen in PGF2 receptor
knockout mice. By using cyclosporin A and PGF2
treatment, we established that inhibition of NUR77 DNA binding in
vivo prevents PGF2 induction of the 20-HSD gene
in the corpus luteum. Taken together, our results demonstrate,
for the first time, that PGF2 induces in the corpus
luteum the expression of the nuclear orphan receptor and transcription
factor, NUR77, which in turn leads to the transcriptional stimulation
of 20-HSD, triggering the decrease in serum progesterone essential
for parturition.
*
This work was supported by National Institutes of Health
Grants HD11119 and HD12356, the Schering Foundation, and CONICET, Argentina.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence and requests for reprints should be
addressed: Dept. of Physiology and Biophysics (M/C 901), University of
Illinois, 835 S. Wolcott Ave., Chicago, IL 60612-7342. Fax: -312-413-0159; E-mail: ggibori@uic.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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