Influence of Tumor Necrosis Factor-alpha on the Secretion of Estradiol, Progesterone, Insulin-like Growth Factor-II, Insulin-like Growth Factor Binding Protein-1, 2, 3 in Cultured Human Luteinized Granulosa Cells / 대한산부인과학회잡지

ABSTRACT

OBJECTIVES: To investigate the influence of TNF-alpha on the secretion of estradiol (E2), progesterone (P4), insulin-like growth factor (IGF)-II, insulin-like growth factor binding protein (IGFBP)-1, 2, and 3 in cultured human luteinized granulosa cells MATERIALS AND METHODS: Human luteinized granulosa cells were obtained from the follicular fluid by transvaginal oocyte aspiration from infertile patients undergoing controlled ovarian hyperstimulation (COH) for in vitro fertilization (IVF). The cells were grouped into the control, 1.0, 10.0, and 100.0 ng/ml of TNF-alpha group according to the concentrations of TNF-alpha. The cells were cultured for 72 hours with the different concentrations of TNF-alpha as descibed above. The cells not treated with TNF-alpha served as control. The concentrations of E2, P4, IGF-I, IGFBP-1, 2, and 3 were determined in conditioned culture media by immunoradiometric assay (IRMA) or radioimmunoassay (RIA). RESULTS: The cell number in 100.0 ng/ml of TNF-alpha group was significantly higher than those in other groups, although the cell viabilities were similar in all groups. There were no statistically significant differences in the concentrations of E2 in all groups. However, the concentrations of P4 were seemed to be decreased as the concentrations of TNF-alpha were increased and the concentration of P4 in 100.0 ng/ml of TNF-alpha group was significantly lower than those in the control and other TNF-alpha groups. The concentrations of IGF-II, IGFBP-1, 2, and 3 were not different among the control and each TNF-alpha group. The secretion of E2 and P4 was not affected by IGF type I receptor antibody pretreatment. CONCLUSION: TNF-alpha might play a role as a regulator of ovarian physiology by modulating luteinized granulosa cellular proliferation and P4 secretion, and this mechanism might not be related to IGF system.