Follicle-stimulating hormone suppressed excessive production of antimullerian hormone caused by abnormally enhanced promoter activity in polycystic ovary syndrome granulosa cells.

OBJECTIVE: To explore: 1) the cause of excessive production of antimullerian hormone (AMH); 2) the effect of FSH on overproduction of AMH; and 3) expression of AMH receptor II (AMHRII) in polycystic ovary syndrome (PCOS) granulosa cells.
DESIGN: Case-control study.
SETTING: University affiliated hospital. MATERIAL(S): The granulosa cells from 8-10-mm follicles were divided into four groups: unstimulated PCOS granulosa cells (n=12), exogenous FSH (5 ng/mL)-stimulated PCOS granulosa cells (n=12), internal FSH (150-300 IU/d)-stimulated PCOS granulosa cells (n=20), and control granulosa cells from non-PCOS infertile patients with regular menstruation (control; n=29). INTERVENTION(S): Exogenous FSH was added into the medium of unstimulated PCOS granulosa cells. MAIN OUTCOME MEASUREMENT(S): The secretory levels and mRNA abundance of AMH, the mRNA and protein levels of AMHRII, and the luciferase activity of AMH. RESULT(S): Both the secretiory level and mRNA abundance of AMH were significantly enhanced in PCOS granulosa cells. They could be partially suppressed by FSH. The mRNA and protein levels of AMHRII in PCOS granulosa cells were significantly increased. However, they were not affected by FSH. The luciferase activity of AMH in PCOS granulosa cells was significantly amplified but could be suppressed by FSH. CONCLUSION(S): Enhanced promoter activity can cause excessive production of AMH in PCOS granulosa cells. FSH may inhibit the excessive secretion of AMH by suppressing the luciferase activity of AMH promoter, but it has no effect on AMHRII expression.