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血管紧张素II对培养的人颗粒细胞孕酮生成的调节作用。血管紧张素II 2型受体的表达。

Regulatory role of angiotensin II on progesterone production by cultured human granulosa cells. Expression of angiotensin II type-2 receptor.

作者信息

Johnson M C, Vega M, Vantman D, Troncoso J L, Devoto L

机构信息

Institute of Maternal and Child Research, School of Medicine, University of Chile, San Borja-Arriarán Clinical Hospital, Santiago, Chile.

出版信息

Mol Hum Reprod. 1997 Aug;3(8):663-8. doi: 10.1093/molehr/3.8.663.

DOI:10.1093/molehr/3.8.663
PMID:9294849
Abstract

The role of angiotensin II (AngII) in ovarian steroidogenesis is not clearly understood. In order to study its action on progesterone synthesis and to determine which receptor subtype is involve, granulosa cells obtained from women undergoing in-vitro fertilization were cultured for 2 or 4 days and then incubated in the presence of AngII (10(-7) M) with or without human chorionic gonadotrophin (HCG, 10 IU/ml) for 3 or 18 h. In cells cultured for 2 days, incubation with AngII decreased progesterone secretion by 36%, and inhibited activity of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) by 87% (P < 0.05), although its expression was not significantly reduced. However, in cells cultured for 4 days, progesterone production was enhanced by incubation with AngII (38%), and no change was observed in 3 beta-HSD expression. Both inhibitory and stimulatory effects were dose-dependent. Progesterone secretion was increased (93%) by incubation with HCG of cells cultured for 4, but not for 2 days, and no potentiation was observed with AngII. Treatment with PD123177 completely blocked the action of AngII and decreased the HCG-stimulated secretion of progesterone by 27%. Angiotensin type-2 (AT2) receptor mRNA was expressed in cells cultured for 4 days. In conclusion, AngII showed a regulatory role in in-vitro progesterone production by human granulosa luteinized cells, modulating the activity of 3 beta-HSD. It is likely that these actions may be mediated via membrane receptors, possibly of the AT2 receptor family.

摘要

血管紧张素II(AngII)在卵巢类固醇生成中的作用尚不清楚。为了研究其对孕酮合成的作用并确定涉及哪种受体亚型,从接受体外受精的女性中获取的颗粒细胞培养2天或4天,然后在有或无人类绒毛膜促性腺激素(HCG,10 IU/ml)存在的情况下,与AngII(10⁻⁷ M)一起孵育3小时或18小时。在培养2天的细胞中,与AngII孵育可使孕酮分泌减少36%,并使3β-羟基类固醇脱氢酶(3β-HSD)的活性抑制87%(P<0.05),尽管其表达没有显著降低。然而,在培养4天的细胞中,与AngII孵育可使孕酮生成增加(38%),并且3β-HSD表达未观察到变化。抑制和刺激作用均呈剂量依赖性。培养4天但不是2天的细胞与HCG孵育可使孕酮分泌增加(93%),并且与AngII一起未观察到增强作用。用PD123177处理完全阻断了AngII的作用,并使HCG刺激的孕酮分泌减少27%。血管紧张素2型(AT2)受体mRNA在培养4天的细胞中表达。总之,AngII在人颗粒黄体化细胞的体外孕酮生成中发挥调节作用,调节3β-HSD的活性。这些作用可能是通过膜受体介导的,可能是AT2受体家族的膜受体。

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