GONADOTROPIN RECEPTORS OF THE PRIMATE CORPUS-LUTEUM .2. CHANGES IN AVAILABLE LUTEINIZING HORMONE-BINDING AND CHORIONIC GONADOTROPIN-BINDING SITES IN MACAQUE LUTEAL MEMBRANES DURING THE NON-FERTILE MENSTRUAL-CYCLE
GONADOTROPIN RECEPTORS OF THE PRIMATE CORPUS-LUTEUM .2. CHANGES IN AVAILABLE LUTEINIZING HORMONE-BINDING AND CHORIONIC GONADOTROPIN-BINDING SITES IN MACAQUE LUTEAL MEMBRANES DURING THE NON-FERTILE MENSTRUAL-CYCLE
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DOI：
10.1210/endo-110-6-2068
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发表时间：
1982-01-01
期刊：
影响因子：
4.8
通讯作者：
STOUFFER, RL
中科院分区：
文献类型：
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作者：
CAMERON, JL;STOUFFER, RL
用~(125)I-人促黄体激素(~(125)I)/人绒毛膜促性腺激素(HCG)结合15,000次，在非生育月经周期的特定阶段检测了灵长类黄体促性腺激素受体的数量。周期中期黄体生成素高峰后第2、4-5、6-9、10-12、13-15和16-18天的恒河猴黄体组织颗粒分数。可用的黄体生成素受体的数量(最大结合容量)和亲和力(解离常数)由平衡结合数据的Scatchard分析确定。在黄体的整个生命周期中，可用的受体对hLH和hCG都表现出类似的亲和力(解离常数，0.88。+-。0.04倍。10-10和0.79+-。0.03次。分别为10-10M)。相反，受体的数量从黄体早期增加到最高水平(8.9.+-。黄体中期(黄体中期(黄体生成素高峰后6-9天))。黄体重量和血清孕酮含量在黄体生成素高峰后4-5天达到最高水平，之后达到最大黄体生成素结合能力。受体数目显著减少(4.9.+-.0.6f[Femto]molLh/mg；P<；0.05)，在黄体生成素高峰后13-15天下降到低水平，但在月经前后可检测到(2.3.+-)。0.3fmolLh/mg)。虽然黄体切除的8只猴子中有4只在黄体生成素高峰后10-12天孕酮水平下降，但这4个组织的黄体生成素结合能力(9.0+-。2.4fmol/mg)与切除的组织相当，而孕酮仍然升高(8.7±-)。0.8fmol/mg)。因此，黄体重量下降之前，黄体黄体结合能力下降，但似乎是在黄体溶解时循环孕酮早期下降之后。人绒毛膜促性腺激素结合能力的类似变化也发生在黄体的整个寿命中。黄体颗粒组分与10-8M前列腺素F2α的共孵育显著(P<；0.01)抑制[1215I]-HLH摄取，而10~(-8)M前列腺素E_2和雌二醇则无明显作用。在月经周期中，可用黄体生成素受体数量的显著变化，但亲和力的变化，与恒河猴黄体的发育和退化有关。然而，从血清孕酮水平的下降判断，黄体溶解的最初阶段并不一定在可用的黄体生成素受体显著下降之前或与之相关。虽然潜在的黄体溶解药物可能在体外直接调节黄体生成素受体的可获得性，但黄体黄体激素受体的丧失并不是正常诱导月经周期黄体溶解的必需步骤。
The gonadotropin receptor population of the primate corpus luteum was examined at specific stages of the nonfertile menstrual cycle via [125I]iodohuman LH [luteinizing hormone] ([125I]iodo-hLH)/hCG [human chorionic gonadotropin] binding to 15,000 .times. g particulate fractions of luteal tissue obtained from rhesus monkeys 2, 4-5, 6-9, 10-12, 13-15 and 16-18 days after the midcycle LH surge. The number (maximum binding capacity) and affinity (dissociation constant) of available LH-CG receptors were determined from Scatchard analyses of equilibrium binding data. Available receptors displayed comparable affinity for both hLH and hCG throughout the lifespan of the corpus luteum (dissociation constant, 0.88 .+-. 0.04 .times. 10-10 and 0.79 .+-. 0.03 .times. 10-10 M, respectively). In contrast, the number of receptors increased from the early luteal phase to maximal levels (8.9 .+-. 0.75 fmol LH bound/mg tissue) during the midluteal phase (6-9 days post-LH surge) of the cycle. Luteal weight and serum progesterone content reached maximal levels 4-5 days after the LH surge, before the development of maximal LH binding capacity. Receptor number decreased significantly (4.9 .+-. 0.6 f[femto]mol LH/mg; P < 0.05) by 13-15 days after the LH surge and dropped to low, but detectable levels around menses (2.3 .+-. 0.3 fmol LH/mg). Although progesterone levels were declining in 4 of 8 monkeys luteectomized 10-12 days after the LH surge, the LH binding capacity of these 4 tissues (9.0 .+-. 2.4 fmol/mg) was comparable to that of tissues removed while progesterone remained elevated (8.7 .+-. 0.8 fmol/mg). Thus, the decline in LH binding capacity preceded any loss in luteal weight, but appeared to follow the early decline in circulating progesterone at luteolysis. Similar changes in hCG binding capacity also occurred throughout the lifespan of the corpus luteum. Coincubation of luteal particulate fractions with 10-8 M prostaglandin F2.alpha. significantly (P < 0.01) inhibited [1215I]iodo-hLH uptake, whereas 10-8 M prostaglandin E2 and estradiol had no effect. Marked changed in the number, but not the affinity, of available LH-CG receptors are associated with the development and regression of the corpus luteum of the rhesus monkey during the menstrual cycle. However, the initial stages of luteolysis, as judged from declining serum progesterone levels, are not necessarily preceded by or associated with an appreciable decline in available LH-CG receptors. Although potential luteolytic agents may directly modulate LH-CG receptor availability in vitro, the loss of luteal LH receptors is not an obligatory step in the normal induction of luteolysis in the menstrual cycle.