Schteingart H F, Meroni S B, Pellizzari E H, Pérez A L, Cigorraga S B
Centro de Investigaciones Endocrinológicas, Hospital de Niños R. Gutierrez, Buenos Aires, Argentina.
J Steroid Biochem Mol Biol. 1995 Apr;52(4):375-81. doi: 10.1016/0960-0760(94)00181-k.
Sertoli cell aromatase activity is high in very young animals and declines throughout pubertal development. Little is known about the regulatory factors which might be involved in the pronounced decline suffered by this enzymatic activity. In this paper we show that estradiol production in Sertoli cells is dependent on cell density in the culture and that chronic stimulation with hormones can decrease estradiol acute response to FSH. In 8-day-old Sertoli cells cultured at low density (LD: 7.1 +/- 0.3 micrograms DNA), estradiol production was 151 +/- 11 pgE2/micrograms DNA, while in those cultured at high density (HD: 30.3 +/- 0.6 micrograms DNA), production was 30 +/- 5 pgE2/micrograms DNA. Similar results were obtained in 20-day-old Sertoli cell cultures (LD: 57 +/- 4 pgE2/micrograms DNA vs HD: 26.0 +/- 0.6 pgE2/micrograms DNA). On the other hand, treatment of Sertoli cell cultures (8- and 20-day-old) for 96 h, with FSH (100 ng/ml), EGF (50 ng/ml), insulin (10 micrograms/ml) and IGF-I (50 ng/ml) at different densities resulted mostly in inhibition of aromatase activity. The effect caused by FSH was apparently not related to desensitization as aromatization with dbcAMP could not overcome the decreased ability of these cells to produce estradiol. The effect caused by EGF was observed in 8-day-old Sertoli cells cultured under high density conditions. Marked inhibition was observed with insulin and IGF-I in 8-day-old Sertoli cell cultures. Considering previous reports indicating a decrease in Sertoli cell aromatase activity with age, our results suggest a potential role for FSH, EGF, insulin and IGF-I on the Sertoli cell differentiation process which occurs throughout pubertal development.
支持细胞芳香化酶活性在非常年幼的动物中较高，并在整个青春期发育过程中下降。对于可能参与这种酶活性显著下降的调节因子知之甚少。在本文中，我们表明支持细胞中雌二醇的产生取决于培养中的细胞密度，并且激素的慢性刺激会降低支持细胞对促卵泡激素（FSH）的雌二醇急性反应。在低密度（LD：7.1±0.3微克DNA）培养的8日龄支持细胞中，雌二醇产量为151±11 pgE2/微克DNA，而在高密度（HD：30.3±0.6微克DNA）培养的细胞中，产量为30±5 pgE2/微克DNA。在20日龄支持细胞培养物中也获得了类似结果（LD：57±4 pgE2/微克DNA vs HD：26.0±0.6 pgE2/微克DNA）。另一方面，在不同密度下用FSH（100 ng/ml）、表皮生长因子（EGF，50 ng/ml）、胰岛素（10微克/ml）和胰岛素样生长因子-I（IGF-I，50 ng/ml）对支持细胞培养物（8日龄和20日龄）进行96小时处理，大多会抑制芳香化酶活性。FSH引起的效应显然与脱敏无关，因为用二丁酰环磷腺苷（dbcAMP）进行芳香化作用并不能克服这些细胞产生雌二醇能力的下降。在高密度条件下培养 的8日龄支持细胞中观察到了EGF引起的效应。在8日龄支持细胞培养物中，胰岛素和IGF-I产生了明显抑制作用。考虑到先前的报告表明支持细胞芳香化酶活性随年龄下降，我们的结果提示FSH、EGF、胰岛素和IGF-I在整个青春期发育过程中发生的支持细胞分化过程中可能发挥作用。
