Somatomedin C augments FSH-induced differentiation of cultured rat granulosa cells.

Somatomedin C augments FSH-induced differentiation of cultured rat granulosa cells.
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Somatomedin C 增强 FSH 诱导的培养大鼠颗粒细胞的分化。

DOI:
10.1152/ajpendo.1985.249.1.e26
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发表时间:
1985
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Li,CH
Li,CH
中科院分区:
--
文献类型:
--
作者:
Davoren,JB;Hsueh,JW;Li,CH

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大鼠生长激素(GH)缺乏与卵巢类固醇激素对促性腺激素的反应性降低有关,可能是通过GH依赖性生长调节素C/胰岛素样生长因子I(SM C/IGF I)的产生减少。我们研究了合成SM C/IGF I对体外促性腺激素刺激的卵巢类固醇生成的直接影响。颗粒细胞在无血清培养基中培养48 h,加入促卵泡激素(FSH),同时加入或不加入SM C/IGF I。FSH剂量依赖性地增加雌激素和孕酮的产生。SM C/IGF I的伴随治疗导致在所测试的FSH剂量的全范围内,卵泡抑素分泌的剂量依赖性增加,最大增加2.3至2.6倍。FSH刺激的雌激素增加了2.4倍,但只有在低剂量的FSH。SM C/IGF I增强的雌激素生成与增加的雌烯醇酮生成和3 β-羟基类固醇脱氢酶活性相关,而增强的雌激素生成似乎是由于增强的芳香酶活性。SM C/IGF I在生理相关浓度下的作用与细胞外cAMP积累和细胞蛋白含量增加相关,但与细胞数量或活力的任何变化无关。与SM C/IGF I相反,密切相关的肽增殖刺激活性降低了雌激素的产生,同时增加了孕酮代谢产物的积累。本研究结果表明,生长激素依赖肽SM C/IGF I可能发挥作用,在卵巢发育中,通过促进促性腺激素刺激的颗粒细胞类固醇激素的生成。
Growth hormone (GH) deficiency in rats is associated with decreased ovarian steroidal responsiveness to gonadotropins, possibly through a reduction in the production of the GH-dependent Somatomedin C/insulinlike growth factor I (SM C/IGF I). We have investigated the direct effects of synthetic SM C/IGF I on gonadotropin-stimulated ovarian steroidogenesis in vitro. Granulosa cells were cultured in a serum-free medium for 48 h in the presence of follicle-stimulating hormone (FSH), with or without SM C/IGF I. FSH dose-dependently increased both estrogen and progestin production. Concomitant treatment with SM C/IGF I led to a dose-dependent augmentation of progestin secretion over the full range of FSH doses tested, by a maximum of 2.3- to 2.6-fold. FSH-stimulated estrogen was enhanced by up to 2.4-fold but only at low doses of FSH. SM C/IGF I-enhanced progestin production was associated with increased pregnenolone production and 3 beta-hydroxysteroid dehydrogenase activity, whereas augmented estrogen production appeared to be due to enhanced aromatase activity. The actions of SM C/IGF I, at physiologically relevant concentrations were correlated with increased extracellular cAMP accumulation and cellular protein content but were independent of any change in cell number or viability. In contrast to SM C/IGF I, the closely related peptide multiplication-stimulating activity decreased estrogen production while increasing progestin metabolite accumulation. The present results indicate that the GH-dependent peptide SM C/IGF I may play a role in ovarian development by enhancing gonadotropin-stimulated granulosa cell steroidogenesis.
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