CYTOKINE-MEDIATED REGULATION OF OVARIAN-FUNCTION - TUMOR NECROSIS FACTOR-ALPHA INHIBITS GONADOTROPIN-SUPPORTED PROGESTERONE ACCUMULATION BY DIFFERENTIATING AND LUTEINIZED MURINE GRANULOSA-CELLS

被引:134
作者
ADASHI, EY
RESNICK, CE
PACKMAN, JN
HURWITZ, A
PAYNE, DW
机构
[1] Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of Maryland School of Medicine Baltimore, MD
关键词
granulosa cells; ovary; Tumor necrosis factor α;
D O I
10.1016/0002-9378(90)91289-O
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Current views favor the notion that resident ovarian macrophages play an in situ role in the regulation of ovarian function through the local secretion of regulatory molecule(s) (i.e., cytokines). Herein we report on the potential ovarian relevance of one such macrophage product, tumor necrosis factor (TNF) α, a polypeptide capable of oncolytic as well as pleiotropic noncytotoxic biologic activities. Our findings suggest that the ability of TNFα to diminish the gonadotropin-supported accumulation of progesterone by granulosa/luteal cells is largely due to attenuation of key biosynthetic steps leading to progesterone production. These findings are in keeping with the notion that TNFα, possibly of intraovarian (e.g., macrophage or granulosa cell) origin, may comprose the centerpiece of a regulatory loop designed to attenuate gonadotropin hormonal action. Acting at or adjacent to its site of synthesis, TNFα may thus partake in the modulation of ovarian progestin economy, possibly in connection with the death of the corpus luteum. © 1990.
引用
收藏
页码:889 / 899
页数:11
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