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a Department of Anatomy, University of California, San Francisco, California 94143
b Department of Veterinary Biosciences, University of Illinois, Urbana, Illinois 61802
c Department of Cell Biology, Baylor College of Medicine, Houston, Texas 77030
The objective of this study was to determine whether uterine stromal and/or epithelial progesterone receptor (PR) is required for the antagonism by progesterone (P4) of estradiol-17ß (E2) action on expression of PR and lactoferrin in uterine epithelium. Uterine tissue recombinants were prepared with epithelium (E) and stroma (S) from wild-type (wt) and PR knockout (PRKO) mice: wt-S+wt-E and PRKO-S+wt-E. P4 action on epithelial PR expression was studied in wt-S+wt-E and PRKO-S+wt-E tissue recombinants. E2 down-regulated epithelial PR in both types of tissue recombinants, but P4 blocked E2-induced down-regulation of epithelial PR only in wt-S+wt-E tissue recombinants. Thus, P4 requires stromal PR to inhibit E2-induced down-regulation of epithelial PR. Epithelial PR is not sufficient in itself. The inhibitory effect of P4 on lactoferrin expression was studied in 4 types of tissue recombinants (wt-S+wt-E, PRKO-S+wt-E, wt-S+PRKO-E, and PRKO-S+PRKO-E). E2 induced lactoferrin in all 4 types of tissue recombinants. P4 blocked E2-induced lactoferrin expression only in wt-S+wt-E tissue recombinants. In wt-S+PRKO-E tissue recombinants, P4 inhibited lactoferrin expression only partially. P4 failed to block E2-induced lactoferrin expression in PRKO-S+wt-E and PRKO-S+PRKO-E tissue recombinants. Thus, both epithelial and stromal PR are essential for full P4 inhibition of E2-induced lactoferrin expression.
1 Supported by NIH Grants AG-13784 and DK47517, AG-15500 and HD-07857.
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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