Iida S, Widmaier E P, Hall P F
Biochem J. 1986 May 15;236(1):53-9. doi: 10.1042/bj2360053.
The hypothesis that ACTH (corticotropin) stimulates steroidogenesis by a mechanism that involves breakdown of polyphosphoinositides and increase in intracellular Ca2+ (called here the 'phosphatidylinositide-Ca2+ mechanism') was tested in Y-1 adrenal-tumour cells and in bovine fasciculata cells, by using incorporation of 32P and myo-[3H]inositol to study phospholipid metabolism, and quin-2 and fura 2 to measure intracellular Ca2+. As a positive control, we repeated experiments showing that angiotensin II stimulates glomerulosa cells by way of the phosphatidylinositide-Ca2+ mechanism, by using the same methods. With Y-1 and fasciculata cells, no change was observed in the incorporation of either of the labelled precursors into any phosphatidylinositide or into any of three major phosphoinositols, i.e. inositol phosphate, bisphosphate and trisphosphate. Moreover, no change in mass of any of these compounds was seen. No change was observed in the concentration of intracellular Ca2+ in Y-1 or fasciculata cells on addition of ACTH, by using either quin-2 or fura 2. By contrast, decreased incorporation of 32P into phosphatidylinositol bisphosphate and an increase in intracellular Ca2+ were seen when glomerulosa cells were treated with angiotensin II. It is concluded that the phosphatidylinositide-Ca2+ mechanism is not used by Y-1 adrenal or bovine fasciculata cells in the steroidogenic response to ACTH unless the mechanism is radically different from that seen with all other hormones so far tested in which this mechanism occurs.
促肾上腺皮质激素（ACTH）通过涉及多磷酸肌醇分解和细胞内Ca2+增加的机制（在此称为“磷脂酰肌醇 - Ca2+机制”）刺激类固醇生成的假说，在Y - 1肾上腺肿瘤细胞和牛束状带细胞中进行了验证。通过掺入32P和肌醇 - [3H]肌醇来研究磷脂代谢，并用喹啉 - 2和fura 2来测量细胞内Ca2+。作为阳性对照，我们使用相同方法重复了实验，结果表明血管紧张素II通过磷脂酰肌醇 - Ca2+机制刺激球状带细胞。对于Y - 1细胞和束状带细胞，未观察到任何一种标记前体掺入任何磷脂酰肌醇或三种主要磷酸肌醇（即肌醇磷酸、二磷酸和三磷酸）中的情况发生变化。此外，这些化合物的质量也未发生变化。使用喹啉 - 2或fura 2时，在添加ACTH后，Y - 1细胞或束状带细胞内Ca2+浓度未观察到变化。相比之下，当用血管紧张素II处理球状带细胞时，观察到32P掺入磷脂酰肌醇二磷酸减少，细胞内Ca2+增加。结论是，Y - 1肾上腺细胞或牛束状带细胞在对ACTH的类固醇生成反应中不使用磷脂酰肌醇 - Ca2+机制，除非该机制与迄今为止测试的所有其他发生此机制的激素的机制截然不同。
