5 years ago

Basal cells show increased expression of aromatase and estrogen receptor α in prostate epithelial lesions of male aging rats.

Monica Morais-Santos, Hipácia Werneck-Gomes, Cleida A Oliveira, Leticia C Santos, Gabriel H Campolina-Silva, Rex A Hess, Germán A B Mahecha
Besides androgens, estrogen signaling plays key role in normal development and pathologies of the prostate. Irreversible synthesis of estrogens from androgens is catalyzed by aromatase. Interestingly, animals lacking aromatase do not develop cancer or prostatitis, whereas those with overexpression of aromatase and consequently high estrogen levels, develop prostatitis and squamous metaplasia via estrogen receptor 1 (ERα). Even with this evidence, the aromatase expression in the prostate is controversial. Moreover, little is known about the occurrence of age-dependent variation of aromatase and its association with histopathological changes commonly found in advanced age, a knowledge gap that is addressed herein. For this purpose, the immunoexpression of aromatase was evaluated in the prostatic complex of young adult to senile Wistar rats. ERá was also investigated to extend our understanding of estrogen responsiveness in the prostate. Moderate cytoplasmic immunoreactivity for aromatase was detected in the glandular epithelium. Eventually, some basal cells showed intense staining for aromatase. The expression pattern for aromatase appeared similar in the normal epithelium when young and senile rats were compared, a result corroborated by Western blotting. Conversely, in senile rats, there was an increase in the frequency of basal cells intensely stained for aromatase, which appeared concentrated in areas of intraepithelial proliferation and prostatitis. These punctual areas also presented increased ERα positivity. Together, these findings point out a plausible source for hormonal imbalance, favoring the estrogen production, which by acting through ERα, may favor the development of prostatic lesions commonly found in advanced ages.

Publisher URL: http://doi.org/10.1210/en.2017-00773

DOI: 10.1210/en.2017-00773

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