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This version published online on October 13, 2005
Endocrinology, doi:10.1210/en.2005-0683
A more recent version of this article appeared on January 1, 2006
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Submitted on June 7, 2005
Accepted on October 3, 2005

17{beta}-estradiol induces apoptosis in the developing rodent prostate independently of ER{alpha} or ER{beta}

R A Taylor, P Cowin, J F Couse, K S Korach, and G P Risbridger*

Monash Institute of Reproduction & Development, Monash University, Clayton, Victoria, Australia, 3168 (RAT, PC, GPR); Department of Environmental and Molecular, Toxicology, North Carolina State University, Raleigh, North Carolina 27695 (JFC); Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences/National Institutes of Health, Research Triangle Park, North Carolina 27709 (JFC, KSK)

* To whom correspondence should be addressed. E-mail: gail.risbridger{at}med.monash.edu.au.

Estrogens induce both proliferative and anti-proliferative responses in the prostate gland. To date, anti-proliferative effects of estrogens are generally considered to be due to systemic anti-androgenic actions. However, estrogen action mediated through ER{beta} was recently suggested as another mechanism of induction of apoptosis in the prostate. This study aimed to explore the hypothesis that the anti-proliferative effects of estrogen are directly mediated through ER{beta} using a prostate organ culture system. We previously reported effects of 17{beta}-estradiol (E2) using rat ventral prostate (VP) tissues, and adapted the system for culturing mouse tissues. In both rat and mouse models, estrogen-induced apoptosis was detected that was spatially and regionally localized to the epithelium of the distal tips. Using organ cultures of {alpha}ERKO and {beta}ERKO prostates, we failed to demonstrate that apoptosis induced by E2 was mediated through either receptor subtype. Activation of estrogen receptor selective ligands (ER{alpha}: propyl pyrazole triol (PPT); ER{beta}, diaryl-proprionitrile (DPN) and 5{alpha}-androstane-3{beta},17{beta}-diol (3{beta}Adiol)) in organ culture experiments failed to induce apoptosis, as did the membrane impermeable conjugate E2:BSA, discounting the possibility of non-genomic effects. Consequently, E2 regulation of androgen receptor (AR) expression was examined and in the presence of nanomolar (nM) testosterone levels, E2 caused a specific reduction in AR protein expression in wild-type, {alpha}ERKO and {beta}ERKO mice, particularly in the distal region where apoptosis was detected. This down-regulation of AR protein provides a possible mechanism for the pro-apoptotic action of E2 that is independent of estrogen receptors or non-genomic effects.
Key words: prostate • estrogen • estrogen receptor knockout (ERKO) • apoptosis • androgen receptor




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