Nongenomic effects of androstenedione on human granulosa luteinizing cells
Nongenomic effects of androstenedione on human granulosa luteinizing cells
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DOI：
10.1210/jc.83.1.263
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发表时间：
1998-01-01
影响因子：
5.8
通讯作者：
Tesarik, J
中科院分区：
文献类型：
--
作者：
Machelon, V;Nomé, F;Tesarik, J
本研究考察了雄激素对人颗粒黄体化细胞中胞质游离 Ca2+ 浓度 ([Ca2+]i) 的快速（5-60 秒）影响。从人类排卵前卵泡获得细胞，并使用 Ca2+ 响应荧光染料 Fluo-3 测量 [Ca2+]i。摩尔浓度在 100 pmol/L 和 1 mu mol/L 之间的雄烯二酮在添加到细胞后 5 秒内增加 [Ca2+]i。这种 [Ca2+]i 增加是由于 Ca2+ 流入（如乙二醇-双（对氨基乙基醚）-N,N,N',N'-四乙酸和电压依赖性 Ca2+ 通道阻滞剂维拉帕米的作用）和 Ca2+ 从内质网动员（如毒胡萝卜素的作用）所致。用百日咳毒素和 U-73,122（一种磷脂酶 C 特异性抑制剂）治疗，消除了雄烯二酮对 [Ca2+]i 的影响。 Flutamide 是一种核雄激素受体拮抗剂，不能阻断雄烯二酮诱导的 [Ca2+]i 增加。睾酮（100 pmol/L 至 1 mumol/L）没有效果。这是第一份表明雄烯二酮增加颗粒细胞中 [Ca2+]i 的报告。这些数据为颗粒细胞中存在一种新的、短期的雄烯二酮作用机制提供了证据，该机制涉及质膜中的电压依赖性 Ca2+ 通道和通过百日咳毒素敏感的 G 蛋白激活磷脂酶 C。
This study examines rapid (5-60 s) effects of androgens on the cytosolic free Ca2+ concentration ([Ca2+]i) in human granulosa luteinizing cells. Cells were obtained from human preovulatory follicles, and [Ca2+]i was measured with the use of the Ca2+-responsive fluorescent dye fluo-3. Molar concentrations between 100 pmol/L and 1 mu mol/L androstenedione increased [Ca2+]i within 5 s after addition to cells. This [Ca2+]i increase resulted from both Ca2+ influx, as shown by the effects of ethyleneglycol-bis-(p-amino ethyl ether)-N,N,N',N'-tetraacetic acid and the voltage-dependent Ca2+ channel blocker verapamil, and Ca2+ mobilization from the endoplasmic reticulum, as shown by the effects of thapsigargin. Treatment with pertussis toxin and U-73,122, a specific inhibitor of phospholipase C, abolished the effects of androstenedione on [Ca2+]i. Flutamide, a nuclear androgen receptor antagonist, did not block the increase in [Ca2+]i induced by androstenedione. Testosterone (100 pmol/L to 1 mu mol/L) had no effect. This is the first report showing that androstenedione increases [Ca2+]i in granulosa cells. These data provide evidence for the presence in granulosa cells of a novel, short term mechanism of androstenedione action involving voltage-dependent Ca2+ channels in the plasma membrane and phospholipase C activation via a pertussis toxin-sensitive G protein.