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Institute of Reproduction and Development, Monash Medical Center, Clayton, Melbourne, Victoria 3168, Australia; Department of Urology, Monash Medical Center, Monash University (M.F.), Clayton, Victoria 3168, Australia; and Department of Anatomy, University of California (G.C.), San Francisco, California 94143
Address all correspondence and requests for reprints to: Dr. Gail Risbridger, Center for Urological Research, Monash Institute of Reproduction and Development, Monash Medical Center, 246 Clayton Road, Clayton, Victoria 3168, Australia. E-mail: gail.risbridger{at}med.monash.edu.au
The exogenous administration of estrogens to male mice alters the
hypothalamic-pituitary-gonadal axis and reduces androgen levels,
leading to a regression of the prostatic epithelium. As well, a
specific direct response to estrogens is the induction of epithelial
squamous metaplasia. The aims of this study were to identify the
process by which the prostatic epithelium is transformed in intact
adult male mice using the synthetic estrogen, diethylstilbestrol. A
comparison of the effects of diethylstilbestrol in the three lobes
revealed a hierarchy of response, with the anterior lobe being the most
responsive, the dorsolateral lobe less responsive, and the ventral lobe
the least responsive. The effect of castration was used to distinguish
between the epithelial responses to estrogen administration and
androgen deprivation. The results demonstrate that transformation of
the epithelium involved proliferation of cells with a basal cell
phenotype, the onset of cytokeratin 10 expression, up-regulation of
progesterone receptor expression, and loss of the cell cycle inhibitor,
p27Kip1 expression; none of these changes was observed
after castration. Mice lacking functional estrogen receptor 
failed
to respond, demonstrating a requirement for estrogen receptor in
the epithelium and/or stroma to mediate the proliferative response to
estrogen in the prostate gland.
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