CYTOKINE-MEDIATED REGULATION OF OVARIAN-FUNCTION - TUMOR NECROSIS FACTOR-ALPHA INHIBITS GONADOTROPIN-SUPPORTED PROGESTERONE ACCUMULATION BY DIFFERENTIATING AND LUTEINIZED MURINE GRANULOSA-CELLS
CYTOKINE-MEDIATED REGULATION OF OVARIAN-FUNCTION - TUMOR NECROSIS FACTOR-ALPHA INHIBITS GONADOTROPIN-SUPPORTED PROGESTERONE ACCUMULATION BY DIFFERENTIATING AND LUTEINIZED MURINE GRANULOSA-CELLS
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DOI：
10.1016/0002-9378(90)91289-o
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发表时间：
1990-04-01
影响因子：
9.8
通讯作者：
PAYNE, DW
中科院分区：
文献类型：
--
作者：
ADASHI, EY;RESNICK, CE;PAYNE, DW
目前的观点倾向于这样的观点：常驻卵巢巨噬细胞通过局部分泌调节分子（即，细胞因子）。在此，我们报道了一种这样的巨噬细胞产物，肿瘤坏死因子（TNF）α，一种能够溶瘤以及多效性非细胞毒性生物活性的多肽。我们的发现提示TNF α的能力。减少颗粒细胞/黄体细胞的促性腺激素支持的孕酮积累主要是由于导致孕酮产生的关键生物合成步骤的减弱。这些发现与TNF α，可能是卵巢内的（例如，巨噬细胞或颗粒细胞）起源，可包括设计用于减弱促性腺激素激素作用的调节环的中心部分。在合成部位或合成部位附近起作用的。TNF.alpha.因此可能参与调节卵巢黄体生成素的经济，可能与黄体的死亡有关。
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) .alpha., a polypeptide capable of oncolytic as well as pleiotropic noncytotoxic biologic activities. Our findings suggest that the ability of TNF.alpha. 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 TNF.alpha., possibly of intraovarian (e.g., macrophage or granulosa cell) origin, may comprise the centerpiece of a regulatory loop designed to attenuate gonadotropin hormonal action. Acting at or adjacent to its site of synthesis. TNF.alpha. may thus partake in the modulation of ovarian progestin economy, possibly in connection with the death of the corpus luteum.