Testosterone effect on the expression of genes that mediate testosterone metabolism and genes that mediate the effect of those metabolites on the prostate
Autor: | F Shidaifat, Young C. Lin |
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Rok vydání: | 2012 |
Předmět: |
Male
medicine.medical_specialty Proliferation index Down-Regulation Estrogen receptor Biology Polymerase Chain Reaction General Biochemistry Genetics and Molecular Biology Prostate cancer Dogs 3-Oxo-5-alpha-Steroid 4-Dehydrogenase Prostate Internal medicine Gene expression medicine Animals Estrogen Receptor beta Testosterone RNA Messenger Prostate gland growth General Pharmacology Toxicology and Pharmaceutics Cell Proliferation General Medicine medicine.disease Up-Regulation Androgen receptor Endocrinology medicine.anatomical_structure Receptors Androgen Steroid Hydroxylases Androgens Signal Transduction |
Zdroj: | Life Sciences. 91:194-198 |
ISSN: | 0024-3205 |
DOI: | 10.1016/j.lfs.2012.07.012 |
Popis: | Aims The aim of this study was to investigate the effect of testosterone treatment on the proliferation index and the mRNA expression levels of 5α-reductase, CYP7B1, androgen receptor (AR), and estrogen receptor β (ERβ) in the canine prostate. Main methods Immature dogs were treated with testosterone for one month, after which prostate gland growth was assessed by comparing the proliferation index in prostates from testosterone-treated dogs with that of untreated control dogs. The relative mRNA expression levels of the aforementioned genes in the prostate glands of testosterone-treated and untreated dogs were determined by real time PCR. Key findings Testosterone treatment induced a highly significant reduction in proliferation index in prostate gland. This inhibition of prostate gland growth was associated with differential mRNA expression of 5α-reductase, CYP7B1, AR, and ERβ by the prostate gland of testosterone-treated dogs, as compared to that of untreated dogs. While the expression levels of 5α-reductase and CYP7B1 mRNA were significantly down-regulated by testosterone treatment, the expression level of ER-β mRNA was highly up-regulated. In contrast, AR mRNA expression was not significantly altered. Significance Prostate gland proliferation appeared to be associated with the expression levels of genes that encode proteins that control intra-prostatic levels of testosterone metabolites and their respective receptors. Testosterone treatment may regulate gene expression in the prostate to generate a phenotype that suppresses growth-promoting signaling through AR and enhances anti-proliferative signaling through ERβ. Therefore, targeting disturbances of this genetic machinery in benign prostate hyperplasia and prostate cancer is of a therapeutic potential. |
Databáze: | OpenAIRE |
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