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The effect of high concentrations of testosterone on ovarian follicle development was investigated. Primary follicles and granulosa cells were cultured in vitro in media supplemented with a testosterone concentration gradient. The combined effects of testosterone and follicle-stimulating hormone(FSH) on follicular growth and granulosa cell gonadotropin receptor m RNA expression were also investigated. Follicle growth in the presence of high testosterone concentrations was promoted at early stages(days 1–7),but inhibited at later stage(days 7–14) of in vitro culture. Interestingly,testosterone-induced follicle development arrest was rescued by treatment with high concentrations of FSH(400 m IU/m L). In addition,in cultured granulosa cells,high testosterone concentrations induced cell proliferation,and increased the m RNA expression level of FSH receptor(FSHR),and luteinized hormone/choriogonadotropin receptor. It was concluded that high concentrations of testosterone inhibited follicle development,most likely through regulation of the FSH signaling pathway,although independently from FSHR downregulation. These findings are an important step in further understanding the pathogenesis of polycystic ovary syndrome.
The effect of high concentrations of testosterone on ovarian follicle development was investigated. Primary follicles and granulosa cells were cultured in vitro in media supplemented with a testosterone concentration gradient. The combined effects of testosterone and follicle-stimulating hormone (FSH) on follicular growth and granulosa Follicle growth in the presence of high testosterone concentrations was promoted at early stages (days 1-7), but inhibited at later stage (days 7-14) of in vitro culture. Interestingly, testosterone -induced follicle development arrest was rescued by treatment with high concentrations of FSH (400 m IU / mL). In addition, in cultured granulosa cells, high testosterone concentrations induced cell proliferation, and increased the m RNA expression level of FSH receptor (FSHR ), and luteinized hormone / choriogonadotropin receptor. It was concluded that high concentrations of testosterone inhibited folli cle development, most likely through regulation of the FSH signaling pathway, although independently from FSHR downregulation. These findings are an important step in further understanding the pathogenesis of polycystic ovary syndrome.