4.3 Article

Differential expression of androgen, estrogen, and progesterone receptors in benign prostatic hyperplasia

Journal

BOSNIAN JOURNAL OF BASIC MEDICAL SCIENCES
Volume 16, Issue 3, Pages 201-208

Publisher

ASSOC BASIC MEDICAL SCI FEDERATION BOSNIA & HERZEGOVINA SARAJEVO
DOI: 10.17305/bjbms.2016.1209

Keywords

Benign prostatic hyperplasia; androgen receptor; estrogen receptor alpha; estrogen receptor beta; progesterone receptor; rat model

Funding

  1. National Nature Science Foundation of China [81470985, 81270842]
  2. Nature Science Foundation for Young Scholars of Gansu province, China [1308RJYA097]

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This study aimed to identify the differential expression levels of androgen receptor (AR), estrogen receptors (ER alpha, ER beta), 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; ER alpha was distributed mainly to stromal cells, but not exclusively; ER beta 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 ER alpha and increased expression of PGR, but no difference in the expression of ER beta 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 ER alpha in BPH, which indicate a promoting role of AR and PGR and an inhibitory role of ER alpha in the pathogenesis of BPH.

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