Protein kinase C mediated regulation of calcium channels in PC-12 pheochromocytoma cells.
Protein kinase C mediated regulation of calcium channels in PC-12 pheochromocytoma cells.
复制标题
蛋白激酶 C 介导 PC-12 嗜铬细胞瘤细胞中钙通道的调节。
DOI：
10.1016/0006-291x(86)90391-8
复制
发表时间：
1986
影响因子：
3.1
通讯作者：
Miller,RJ
中科院分区：
文献类型：
--
作者：
Harris,KM;Kongsamut,S;Miller,RJ
用K+去极化PC-12嗜铬细胞瘤细胞，可立即增加儿茶酚胺的释放。释放的刺激可被Co2+、细胞外钙的清除或二氢吡啶类药物如尼群地平所阻断。其他二氢吡啶类药物如BAY K8644可促进药物释放。释放伴随着电压依赖性的45Ca~(2+)摄取，这种摄取也被Co2+或尼群地平阻断，并被Bay K8644增强。佛波酯佛波酯在10−9~10−6M范围内对儿茶酚胺的释放无明显影响，但可增强K+诱发的儿茶酚胺的释放。一种不能激活蛋白激酶C的TPA类似物无效。相反，相同浓度范围的TPA可阻断70 mM K+或70 mM K+/Bay K8644.45Ca~(2+)引起的45Ca~(2+)内流，TPA不能阻断A23187引起的45Ca~(2+)内流。结果表明，蛋白激酶C可能通过该系统调节分泌细胞的递质输出。
Depolarization of PC-12 pheochromocytoma cells with K+produces an immediate increase in catecholamine release. The stimulation of release is blocked by Co2+, removal of extracellular Ca2+or by dihydropyridine drugs such as nitrendipine. Release is enhanced by other dihydropyridines such as BAY K8644. Release is accompanied by a voltage dependent uptake of45Ca2+which is also blocked by Co2+or nitrendipine and enhanced by BAY K8644. The phorbol ester phorbol 12-myristate-13-acetate (TPA) in the range 10−9– 10−6M produced little effect by itself but augmented the K+evoked release of catecholamine. An analog of TPA which does not activate protein kinase C was ineffective. In contrast, TPA in the same concentration range blocked influx of45Ca2+induced by 70 mM K+or 70 mM K+/ BAY K8644.45Ca2+influx produced by A23187 was not blocked by TPA. The results suggest a system by which protein kinase C may regulate the output of transmitters from secretory cells.