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Monash Institute of Reproduction and Development, Monash University, Monash Medical Center, Clayton, Victoria 3168, Australia; Department of Anatomy, University of California School of Medicine K.A.T., G.R.C.), San Francisco, California 94143; and Department of Urology, University of Illinois College of Medicine (G.S.P.), Chicago, Illinois 60612
Address all correspondence and requests for reprints to: Dr. G. P. Risbridger, 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
Neonatal exposure to high doses of estrogen results in permanent
suppression of prostate growth and reduced sensitivity to androgens in
adulthood. It is unclear whether alterations in prostate growth are due
to a direct effect of estrogens on the gland or are the result of
hypothalamic-pituitary-gonadal axis suppression and a subsequent
reduction in androgen levels. Therefore, the aim of this study was to
determine whether estrogens have a direct effect on the prostate using
a defined method of culturing neonatal prostates. Newborn rat ventral
prostates were microdissected and cultured in the presence of
testosterone, which resulted in branching morphogenesis and ductal
canalization. Solid cords of epithelium differentiated into acini lined
by tall columnar epithelial cells; these acini were surrounded by
stromal cells, expressing smooth muscle 
-actin. When cultured in the
presence of 17ß-estradiol or diethylstilbestrol in addition to
testosterone, androgen-induced prostatic growth was reduced, and
differentiation was altered. Although estrogen-treated explants were
smaller than controls, quantification of epithelial, stromal, and
luminal volumes using unbiased stereology revealed significant changes;
the proportion of epithelial cells and lumen decreased, and the
proportion of stroma increased compared with control values. Concurrent
with this reduced growth rate, we observed a disturbance in the
branching pattern and a reduction in ductal canalization. Specifically,
stromal differentiation and organization were disrupted, so that a
discontinuous smooth muscle layer was observed around the epithelial
ducts, and epithelial differentiation was altered. The effects of
estrogens were not accompanied by a decrease in androgen response via
the androgen receptor, because immunolocalization of this receptor
remained constant. These data demonstrate that high doses of estrogens
are growth inhibitory and have direct effects on prostate development
in vitro, which may occur in vivo in
addition to indirect effects via suppression of the
hypothalamic-pituitary-gonadal axis.
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