Abstract
This study aimed to identify the differential expression levels of androgen receptor (AR), estrogen receptors (ERα, ERβ), and progesterone receptor (PGR) between normal prostate and benign prostatic hyperplasia (BPH). The combination of immunohistochemistry, quantitative real-time reverse transcription polymerase chain reaction, and Western blotting assay was used to identify the distribution and differential expression of these receptors at the immunoactive biomarker, transcriptional, and protein levels between 5 normal human prostate tissues and 40 BPH tissues. The results were then validated in a rat model of BPH induced by testosterone propionate and estradiol benzoate. In both human and rat prostate tissues, AR was localized mainly to epithelial and stromal cell nuclei; ERα was distributed mainly to stromal cells, but not exclusively; ERβ was interspersed in the basal layer of epithelium, but sporadically in epithelial and stromal cells; PGR was expressed abundantly in cytoplasm of epithelial and stromal cells. There were decreased expression of ERα and increased expression of PGR, but no difference in the expression of ERβ in the BPH compared to the normal prostate of both human and rat. Increased expression of AR in the BPH compared to the normal prostate of human was observed, however, the expression of AR in the rat prostate tissue was decreased. This study identified the activation of AR and PGR and repression of ERα in BPH, which indicate a promoting role of AR and PGR and an inhibitory role of ERα in the pathogenesis of BPH.
Highlights
Benign prostatic hyperplasia (BPH), common in elderly men, is a pathological condition characterized by nonmalignant enlargement of both epithelial and stromal tissues within the prostate gland [1], which contributes to series of urinary voiding problems commonly known as lower urinary tract symptoms (LUTS) [2]
A significantly increased expression of progesterone receptor (PGR), decreased expression of estrogen receptor α (ERα), and no significant difference in the expression of ERβ were identified in the BPH group compared to the control group, which indicated the activation of Androgen receptor (AR) and repression of ERα in the rat model of BPH
The present study revealed that the expression of ERα was significantly decreased in the human BPH and rat model of BPH, indicating that ERα might play an inhibitory role in the pathogenesis of BPH rather than a supposed promoting role
Summary
Benign prostatic hyperplasia (BPH), common in elderly men, is a pathological condition characterized by nonmalignant enlargement of both epithelial and stromal tissues within the prostate gland [1], which contributes to series of urinary voiding problems commonly known as lower urinary tract symptoms (LUTS) [2]. The exact molecular mechanisms underlying the induction, maintenance, and development of BPH remain unresolved despite research data from a plethora of studies. The differential expression levels of these receptors between BPH and normal prostate tissues have been controversial, and the exact roles remain unclear [4,5]. Androgen signaling through AR is reported to play a permissive role in the pathogenesis of BPH [6]. A role of estrogen signaling through ERs in the pathogenesis of BPH is supported by increasing evidence from epidemiological, animal, and in vitro studies [4,5,7]. Few researches have revealed the role of PGR in the pathogenesis of BPH [4,8]
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