Talbot J A, Lambert A, Mitchell R, Grabinski M, Anderson D C, Tsatsoulis A, Shalet S M, Robertson W R
Department of Medicine (Clinical Biochemistry), University of Manchester, Hope Hospital, Salford, UK.
Acta Endocrinol (Copenh). 1991 Sep;125(3):280-5. doi: 10.1530/acta.0.1250280.
We have investigated the role of Ca2+ in the control of FSH-induced estradiol secretion by Sertoli cells isolated from 8-10 days old rats. Exogenous Ca2+ (4-8 mmol/l) inhibited FSH-stimulated E2 secretion such that, with 8 mmol/l Ca2+ and FSH (8 IU/l) E2 secretion decreased from 2091 +/- 322 to 1480 +/- 84 pmol/l (p less than 0.002), whilst chelation of Ca2+ in the culture medium with EGTA (3 mmol/l) increased E2 secretion from 360 +/- 45 to 1242 +/- 133 pmol/l) in the absence of FSH. Further, EGTA (3 mmol/l) markedly potentiated FSH (8 IU/l), forskolin (1 mumol/l) and dibutyryl cAMP (1 mmol/l)-stimulated E2 secretion. Addition of the Ca2+ ionophores, ionomycin (2-5 mumol/l) and A23187 (2 mumol/l), inhibited FSH (8 IU/l)-stimulated E2 secretion by greater than 80%. The effect of ionomycin was totally reversible, whereas that of A23187 was irreversible. Ionomycin (5 mumol/l) had no effect on EGTA-induced E2 secretion in the absence of FSH, but reduced EGTA-provoked E2 secretion by 59% in the presence of FSH (8 IU/l). Similarly, forskolin- and dibutyryl cAMP-provoked E2 production was inhibited 46-50% by ionomycin (5 mumol/l). We conclude that FSH-induced E2 secretion from immature rat Sertoli cells is modulated by intra- and extracellular Ca2+.
我们研究了钙离子在控制从8至10日龄大鼠分离的支持细胞中促卵泡激素（FSH）诱导的雌二醇分泌中的作用。外源性钙离子（4 - 8 mmol/L）抑制FSH刺激的E2分泌，以至于在8 mmol/L钙离子和FSH（8 IU/L）存在的情况下，E2分泌从2091±322降至1480±84 pmol/L（p＜0.002），而在无FSH时，用乙二醇双（2-氨基乙基醚）四乙酸（EGTA，3 mmol/L）螯合培养基中的钙离子可使E2分泌从360±45增加至1242±133 pmol/L。此外，EGTA（3 mmol/L）显著增强FSH（8 IU/L）、福斯高林（1 μmol/L）和二丁酰环磷腺苷（1 mmol/L）刺激的E2分泌。添加钙离子载体离子霉素（2 - 5 μmol/L）和A23187（2 μmol/L）可抑制FSH（8 IU/L）刺激的E2分泌达80%以上。离子霉素的作用完全可逆，而A23187的作用不可逆。离子霉素（5 μmol/L）在无FSH时对EGTA诱导的E2分泌无影响，但在有FSH（8 IU/L）时可使EGTA引发的E2分泌减少59%。同样，离子霉素（5 μmol/L）可使福斯高林和二丁酰环磷腺苷引发的E2分泌抑制46 - 50%。我们得出结论，未成熟大鼠支持细胞中FSH诱导的E2分泌受细胞内和细胞外钙离子调节。
