Protein kinase C modulates effects of prostanoids on cyclic adenosine monophosphate in guinea pig chief cells.
Protein kinase C modulates effects of prostanoids on cyclic adenosine monophosphate in guinea pig chief cells.
复制标题
蛋白激酶 C 调节前列腺素类药物对豚鼠主细胞中环磷酸腺苷的影响。
DOI：
10.1002/jcp.1041400112
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发表时间：
1989
影响因子：
5.6
通讯作者：
Cosowsky,L
中科院分区：
文献类型：
--
作者：
Raufman,JP;Cosowsky,L
在检测蛋白激酶C在豚鼠胃分散主细胞信号转导中的作用的过程中，我们观察到phorbol酯抑制前列腺素（PG）刺激的环磷酸腺苷（cAMP）的增加。Phorbol 12 -肉豆蔻酸酯13 -醋酸酯（PMA）是一种蛋白激酶C的活化剂，可使PGE2刺激的cAMP最大水平降低40%。这种剂量依赖性效应在30秒内观察到，并在37°C孵育1分钟时达到最大。不激活蛋白激酶C的药物没有这种效果。添加蛋白激酶C抑制剂H7可消除PMA的抑制作用。添加磷酸二酯酶抑制剂并没有改变PMA的抑制作用，表明这些作用不是由环核苷酸磷酸二酯酶的激活引起的。PMA不改变由霍乱毒素、福斯克林、分泌素或血管活性肠肽引起的细胞cAMP升高。因此，蛋白激酶C的这些前列腺素特异性作用位点似乎不是刺激或抑制鸟嘌呤核苷酸结合蛋白或腺苷酸环化酶系统的催化成分。在分散的主细胞中，蛋白激酶C的激活可能通过直接作用于前列腺素受体来抑制前列腺素诱导的腺苷酸环化酶系统的刺激。
In the course of examining the role of protein kinase C in signal transduction in dispersed chief cells from guinea pig stomach, we observed that phorbol esters inhibit prostaglandin (PG)‐stimulated increases in cyclic adenosine monophos‐phate (cAMP). Phorbol 12‐myristate 13‐acetate (PMA), an activator of protein kinase C, decreased maximal levels of PGE2‐stimulated cAMP by 40%. This dose‐dependent effect was observed within 30 sec and was maximal by 1 min of incubation at 37°C. Phorbols that do not activate protein kinase C did not have this effect. Adding H7, a protein kinase C inhibitor, abolished the inhibitory effects of PMA. Adding phosphodiesterase inhibitors did not alter the inhibitory effects of PMA, indicating that these effects are not caused by activation of cyclic nucleotide phosphodiesterases. PMA did not alter the increase in cellular cAMP caused by cholera toxin, forskolin, secretin, or vasoactive intestinal peptide. Hence the site of these prostanoid‐specific actions of protein kinase C does not appear to be stimulatory or inhibitory guanine nucleotide binding proteins or the catalytic component of the adenylyl cyclase system. In dispersed chief cells, activation of protein kinase C may inhibit prostanoid‐induced stimulation of the adenylyl cyclase system by a direct effect on prostaglandin receptors.