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Biology of Reproduction 64, 272-283 (2001)
© 2001 Society for the Study of Reproduction, Inc.

Regular Article

Regulation of Progesterone Receptors and Decidualization in Uterine Stroma of the Estrogen Receptor-{alpha} Knockout Mouse1

Takeshi Kuritaa, Ki-jun Leec, Philippa T.K. Saundersd, Paul S. Cookec, Julia A. Taylore, Dennis B. Lubahne, Cida Zhaoa, Sari Mäkeläf, Jan-Åke Gustafssonf, Rajvir Dahiyab, and Gerald R. Cunha2,a

a Departments of Anatomy and b Urology, University of California, San Francisco, California 94143 c Department of Veterinary Biosciences, University of Illinois, Urbana, Illinois 61802 d MRC Reproductive Biology Unit, Edinburgh, EH3 9ET, United Kingdom e Departments of Biochemistry and Child Health, University of Missouri, Columbia, Missouri 65211 f Department of Medical Nutrition and Biosciences, Karolinska Institute, NOVUM, S-141 86 Huddinge, Sweden

ABSTRACT

Regulation of progesterone receptor (PR) in uterine stroma (endometrial stroma plus myometrium) by estrogen was investigated in estrogen receptor-{alpha} (ER{alpha}) knockout ({alpha}ERKO) mice. 17ß-Estradiol (E2) increased PR levels in uterine stroma of ovariectomized {alpha}ERKO mice, and ICI 182 780 (ICI) inhibited this E2-induced PR expression. Estrogen receptor-ß (ERß) was detected in both uterine epithelium and stroma of wild-type and {alpha}ERKO mice by immunohistochemistry. In organ cultures of {alpha}ERKO uterus, both E2 and diethylstilbestrol induced stromal PR, and ICI inhibited this induction. These findings suggest that estrogen induces stromal PR via ERß in {alpha}ERKO uterus. However, this process is not mediated exclusively by ERß, because in ERß knockout mice, which express ER{alpha}, PR was up-regulated by E2 in uterine stroma. In both wild-type and {alpha}ERKO mice, progesterone and mechanical traumatization were essential and sufficient to induce decidual cells, even though E2 and ER{alpha} were also required for increase in uterine weight. Progesterone receptor was strongly expressed in decidual cells in {alpha}ERKO mice, and ICI did not inhibit decidualization or PR expression. This study suggests that up-regulation of PR in endometrial stroma is mediated through at least three mechanisms: 1) classical estrogen signaling through ER{alpha}, 2) estrogen signaling through ERß, and 3) as a result of mechanical stimulation plus progesterone, which induces stromal cells to differentiate into decidual cells. Each of these pathways can function independently of the others.

FOOTNOTES

First decision: 22 March 2000.

1 Supported by National Institutes of Health grants AG-13784 and DK47517 to G.R.C., AG-15500 to P.S.C., R01-ES08272 to D.B.L., AG-16870 to R.D., and U.S. Army grant DAMD17-97-1-7171 to D.B.L.

2 Correspondence: Gerald R. Cunha, P.O. Box 0452, Department of Anatomy, University of California-San Francisco, San Francisco, CA 94143. FAX: 415 502 2270; gcunha{at}itsa.ucsf.edu




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