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5 alpha-Androstane-3 beta,17 beta-diol 3 beta-diol, an estrogenic metabolite of 5 alpha-dihydrotestosterone, is a potent modulator of estrogen receptor ER beta expression in the ventral prostrate of adult rats



5 alpha-Androstane-3 beta,17 beta-diol 3 beta-diol, an estrogenic metabolite of 5 alpha-dihydrotestosterone, is a potent modulator of estrogen receptor ER beta expression in the ventral prostrate of adult rats



Steroids 72(14): 914-922



Prostate is one of the major targets for dihydrotestosterone (DHT), however this gland is also recognized as a nonclassical target for estrogen as it expresses both types of estrogen receptors (ER), especially ERR. Nevertheless, the concentrations of aromatase and estradiol in the prostate are low, indicating that estradiol may not be the only estrogenic molecule to play a role in the prostate. It is known that DHT can be metabolized to 5 alpha-androstane-3 beta,17 beta-diol (3 beta-diol), a hormone that binds to ERR but not to AR. The concentration of 3 beta-diol in prostate is much higher than that of estradiol. Based on the high concentration of 3 beta-diol and since this metabolite is a physiological ERR ligand, we hypothesized that 3 beta-diol would be involved in the regulation of ERR expression. To test this hypothesis, adult male rats were submitted to castration followed by estradiol, DHT or 3 beta-diol replacement. ERR and AR protein levels in the prostate were investigated by immunohistochemistry and Western blotting assays. The results showed that after castration, the structure of the prostate was dramatically changed and ER beta and AR protein levels were decreased. Estradiol had just minor effects on the parameters analyzed. DHT-induced partial recovery of ERR while it was the most effective inductor of AR expression. Replacement with 3 beta-diol-induced the highest levels of ERR, but was comparatively less effective in recovering the AR expression and the gland structure. These results offer evidence that one functional role of 3 beta-diol in the prostate may be autoregulation of its natural receptor, ERR.

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Accession: 029581390

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PMID: 17854852

DOI: 10.1016/j.steroids.2007.08.001


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