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Endocrinology Vol. 142, No. 6 2443-2450
Copyright © 2001 by The Endocrine Society

ARTICLES

The Metaplastic Effects of Estrogen on Mouse Prostate Epithelium: Proliferation of Cells with Basal Cell Phenotype1

Gail P. Risbridger, Hong Wang, Mark Frydenberg and Gerald Cunha

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 {alpha} failed to respond, demonstrating a requirement for estrogen receptor {alpha} in the epithelium and/or stroma to mediate the proliferative response to estrogen in the prostate gland.




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