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Biology of Reproduction 62, 821-830 (2000)
© 2000 Society for the Study of Reproduction, Inc.

Articles

Paracrine Regulation of Epithelial Progesterone Receptor by Estradiol in the Mouse Female Reproductive Tract1

Takeshi Kuritab, Ki-jun Leec, Paul S. Cookec, Julia A. Taylorc, Dennis B. Lubahnc, and Gerald R. Cunha2,,a

a Department of Anatomy, University of California, San Francisco, California 94143 b Department of Veterinary Biosciences, University of Illinois, Urbana, Illinois 61802 c Departments of Biochemistry and Child Health, University of Missouri, Columbia, Missouri 65211

Regulation of progesterone receptor (PR) by estradiol-17ß (E2) in mouse uterine and vaginal epithelia was studied. In ovariectomized mice, PR expression was low in both vaginal stroma and epithelium, but high in uterine epithelium. E2 induced PR in vaginal epithelium and stroma, but down-regulated PR in uterine epithelium. Analysis of estrogen receptor {alpha} (ER{alpha}) knockout (ERKO) mice showed that ER{alpha} is essential for E2-induced PR expression in both vaginal epithelium and stroma, and for E2-induced down-regulation, but not constitutive expression of PR in uterine epithelium. Regulation of PR by E2 was studied in vaginal and uterine tissue recombinants made with epithelium and stroma from wild-type and ERKO mice. In the vaginal tissue recombinants, PR was induced by E2 only in wild-type epithelium and/or stroma. Hence, in vagina, E2 induces PR directly via ER{alpha} within the tissue. Conversely, E2 down-regulated epithelial PR only in uterine tissue recombinants constructed with wild-type stroma. Therefore, down-regulation of uterine epithelial PR by E2 requires stromal, but not epithelial, ER{alpha}. In vitro, isolated uterine epithelial cells retained a high PR level with or without E2, which is consistent with an indirect regulation of uterine epithelial PR in vivo. Thus, E2 down-regulates PR in uterine epithelium through paracrine mechanisms mediated by stromal ER{alpha}.

First decision: 21 September 1999.

1 Supported by NIH Grants AG-13784 and DK47517 (to G.R.C), AG-15500 (to P.S.C.), and ES-08272 (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; grcunha{at}itsa.ucsf.edu




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