Audy M C, Boucher Y, Bonnin M
Laboratoire Neurophysiologie, Universite Bordeaux II.
Endocrinology. 1990 Mar;126(3):1396-402. doi: 10.1210/endo-126-3-1396.
The involvement of protein kinase C (PKC) in GnRH action is still a matter of controversy. We have conducted a comparative study of LH and FSH release in response to GnRH and to phorbol ester myristate acetate (PMA), an activator of PKC, by rat pituitary cells maintained in culture. The effect of E2 pretreatment coupled or not with PKC depletion was also studied. Different kinetics in the response of LH and FSH to GnRH were observed, suggesting that the intracellular pathways involved in the release process of the two hormones were somewhat different. Moreover, PMA (10 nM) stimulated LH release greatly and FSH release only slightly. Intracellular PKC depletion, obtained by a prolonged treatment (18 h) of the cells with PMA (1 microM), produced different results according to the endocrine status of the pituitary cells. GnRH (10 nM)-induced LH release was significantly decreased in PKC-depleted cells from proestrous females. For PKC-depleted cells from OVX females, it was decreased significantly only when cells had been pretreated by E2. These results suggest that the modulation of LH secretion by E2 involves PKC activation. FSH release was poorly stimulated by PMA; but, under any conditions, PKC depletion did not affect GnRH-induced FSH release.
蛋白激酶C（PKC）在促性腺激素释放激素（GnRH）作用中的参与情况仍存在争议。我们对培养的大鼠垂体细胞中，促黄体生成素（LH）和促卵泡生成素（FSH）对GnRH以及PKC激活剂佛波酯肉豆蔻酸酯乙酸酯（PMA）的释放反应进行了比较研究。还研究了雌激素（E2）预处理联合或不联合PKC耗竭的效果。观察到LH和FSH对GnRH反应的不同动力学，表明这两种激素释放过程中涉及的细胞内途径有所不同。此外，PMA（10 nM）极大地刺激了LH释放，而对FSH释放的刺激很小。通过用PMA（1 microM）对细胞进行长时间处理（18小时）获得细胞内PKC耗竭，根据垂体细胞的内分泌状态产生了不同的结果。来自动情前期雌性大鼠的PKC耗竭细胞中，GnRH（10 nM）诱导的LH释放显著降低。对于去卵巢（OVX）雌性大鼠的PKC耗竭细胞，只有在细胞经E2预处理时，LH释放才显著降低。这些结果表明，E2对LH分泌的调节涉及PKC激活。PMA对FSH释放的刺激较弱；但在任何情况下，PKC耗竭均不影响GnRH诱导的FSH释放。
