Davis J S, West L A, Farese R V
Biochem Biophys Res Commun. 1984 Aug 16;122(3):1289-95. doi: 10.1016/0006-291x(84)91232-4.
This report describes the rapid effects of GnRH and an agonist [D-Ala6, des-Gly10] GnRH ethylamide (GnRHa) on polyphosphoinositide metabolism in rat granulosa cells. As indicated by the depletion of cellular levels of 32P-prelabeled triphosphoinositide (TPI) and diphosphoinositide (DPI), GnRHa rapidly stimulated the hydrolysis of TPI and DPI. The effect of GnRHa was maximal at the earliest time point examined (30 sec) and preceded GnRHa-induced increases in labeling of phosphatidylinositol. A specific GnRH antagonist had no effect on TPI or DPI levels, but prevented the polyphosphoinositide depletion induced by GnRH. LH did not stimulate depletion of 32P-polyphosphoinositides. The rapid and specific effects of GnRH on polyphosphoinositide depletion may represent an early and possibly initiating event in the action of GnRH.
本报告描述了促性腺激素释放激素(GnRH)及其激动剂[D-丙氨酸6,去甘氨酸10]GnRH乙酰胺(GnRHa)对大鼠颗粒细胞中多磷酸肌醇代谢的快速影响。如32P预标记的三磷酸肌醇(TPI)和二磷酸肌醇(DPI)细胞水平的消耗所示,GnRHa迅速刺激了TPI和DPI的水解。GnRHa的作用在最早检测的时间点(30秒)达到最大,并先于GnRHa诱导的磷脂酰肌醇标记增加。一种特异性GnRH拮抗剂对TPI或DPI水平没有影响,但可防止GnRH诱导的多磷酸肌醇消耗。促黄体生成素(LH)不会刺激32P-多磷酸肌醇的消耗。GnRH对多磷酸肌醇消耗的快速和特异性作用可能代表了GnRH作用中的一个早期且可能是起始事件。