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Direct Response of the Murine Prostate Gland and Seminal Vesicles to Estradiol

Centre for Urological Research (J.J.B., G.P.R.), Monash University, Clayton, Victoria, 3168, Australia; ANZAC Research Institute (D.J.H.), Concord Hospital and University of Sydney, Sydney, New South Wales, 2139, Australia; and Melbourne Pathology (J.S.P.), Collingwood, Victoria, 3066, Australia

Address all correspondence and requests for reprints to: Professor Gail P. Risbridger, Monash Institute of Reproduction and Development, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria, Australia, 3168. E-mail: gail.risbridger{at}med.monash.edu.au.

In the prostate, testosterone action depends on conversion to bioactive metabolites dihydrotestosterone and 17ß-estradiol (E₂) via the 5-reductase and aromatase enzymes, respectively. Exogenous estrogen inhibits prostate growth by indirect effects caused by suppression of pituitary gonadotropins and testicular testosterone output, but direct effects are less well known. Direct effects of estrogens were evaluated using the hypogonadal (hpg) mouse model, which has postnatal deficiency in gonadotropins and testosterone but remains hormone sensitive. Mature hpg mice were implanted sc with implants filled with E₂. After 6 wk, prostate lobe [anterior prostate (AP) and ventral prostate (VP)] and seminal vesicle (SV) organ volumes were significantly increased (P < 0.05) but remained smaller than wild-type mice. Analysis of the relative volumes (the proportional composition) of each tissue compartment in these organs showed significant increases in cellular and luminal volumes (P < 0.05) in AP (but not VP) and in SVs. Stromal fibroblasts proliferated, whereas smooth muscle cells were reduced in the AP and SVs. In the epithelia, basal cells proliferated and became metaplastic in the AP and VP. In the AP, luminal debris accumulated, together with an inflammatory response, but there was no evidence of malignant changes. The current study unequivocally demonstrates direct proliferative responses to E₂ in the hpg mouse AP and VP lobes and SVs, characterized by discrete lobe-specific changes, including smooth-muscle regression, fibroblast proliferation, inflammation, and basal epithelial cell proliferation and metaplasia.

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