Koch B, Lutz-Bucher B
Institut de Physiologie, UA CNRS 309, Université Louis Pasteur, Strasbourg, France.
Biochem Biophys Res Commun. 1989 Sep 15;163(2):1014-20. doi: 10.1016/0006-291x(89)92323-1.
The possible role of protein kinase C (PKC) in the cyclic AMP-dependent mechanism of action of corticotropin-releasing factor (CRF) on proopiomelanocortin cells of anterior and intermediate pituitary glands was examined after pretreatment of cells in culture with the PKC inhibitor retinal or the phorbol ester PMA, which depletes cell stores of the kinase. We found that these drugs not only abolished ACTH response to PMA and vasopressin, which both activate PKC, but unexpectably also dampened by 80-90% the stimulatory effect of CRF. Cell treatment with retinal failed to prevent CRF-induced accumulation of cyclic AMP. Retinal and PMA pretreatments of intermediate pituitary cells likewise inhibited alpha-MSH secretion stimulated by CRF. These data provide evidence to suggest that the mechanism of action of CRF on pituitary cells involves both cyclic AMP and PKC messenger systems.
在用蛋白激酶C（PKC）抑制剂视黄醛或佛波酯PMA对培养细胞进行预处理后，研究了PKC在促肾上腺皮质激素释放因子（CRF）对垂体前叶和中间叶促阿黑皮素原细胞的环磷酸腺苷（cAMP）依赖性作用机制中可能发挥的作用，其中佛波酯会耗尽细胞内该激酶的储存。我们发现，这些药物不仅消除了促肾上腺皮质激素（ACTH）对PMA和加压素的反应（二者均激活PKC），而且出乎意料地还将CRF的刺激作用减弱了80% - 90%。用视黄醛处理细胞未能阻止CRF诱导的cAMP积累。对视黄醛和PMA进行预处理同样会抑制中间叶垂体细胞中由CRF刺激的α-促黑素细胞激素（α-MSH）分泌。这些数据提供了证据表明，CRF对垂体细胞的作用机制涉及cAMP和PKC信使系统。
