Modification of luteinizing hormone secretion by activators of Ca2+/phospholipid-dependent protein kinase.
Modification of luteinizing hormone secretion by activators of Ca2+/phospholipid-dependent protein kinase.
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DOI：
10.1210/endo-118-5-2053
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发表时间：
1986-05
期刊：
影响因子：
4.8
通讯作者：
J. Turgeon;D. W. Waring
中科院分区：
文献类型：
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作者：
J. Turgeon;D. W. Waring
我们研究了Ca 2 +/磷脂依赖性蛋白激酶（蛋白激酶C）在LH分泌中的作用，使用大鼠垂体前叶片获得在已知阶段的发情周期和体外灌流。促分泌素以10分钟（LHRH）或30分钟（所有其他）脉冲给药。用佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）激活蛋白激酶C，2小时后导致LHRH诱导的LH分泌以浓度（1 nM至1 μ M）和蛋白质合成依赖的方式在发情前期（但不是发情期）垂体中扩增;甘油二酯类似物1-油酰-2-乙酰甘油（OAG）也增强随后的LHRH诱导的分泌。在1 μ M，PMA单独增加LH分泌率，但与LHRH诱导的模式不同; PMA反应的特征受先前暴露于LHRH，发情周期阶段和放线菌酮的影响。用8-溴-cAMP或毛喉素预处理导致随后的LHRH诱导的分泌增加，而不影响基线分泌。如果细胞同时暴露于毛喉素和OAG，而不是8-溴-cAMP和OAG，则增强被抑制。这一初步结果表明蛋白激酶C和cAMP依赖性蛋白激酶在LH分泌调节中可能存在相互作用。我们的结论是，关于LH释放的启动，蛋白激酶C似乎只是一个复杂的介质所需的分泌反应LHRH之一。关于LHRH诱导的释放的放大，蛋白激酶C的激活可能是LHRH自引发反应的一个组成部分。
We investigated the role of Ca2+/phospholipid-dependent protein kinase (protein kinase C) in LH secretion using rat anterior pituitary pieces obtained at known stages of the estrous cycle and superfused in vitro. Secretagogues were administered as 10-min (LHRH) or 30-min (all others) pulses. Activation of protein kinase C with phorbol 12-myristate 13-acetate (PMA) results 2 h later in an amplification of LHRH-induced LH secretion in a concentration (1 nM to 1 microM)-and protein synthesis-dependent manner in proestrous, but not estrous, pituitaries; the diacylglycerol analog 1-oleoyl-2-acetylglycerol (OAG) also augments subsequent LHRH-induced secretion. At 1 microM, PMA alone increases the LH secretory rate, but with a pattern different from that induced by LHRH; the characteristics of the PMA response are affected by prior exposure to LHRH, estrous cycle stage, and cycloheximide. Pretreatment with either 8-bromo-cAMP or forskolin results in augmentation of subsequent LHRH-induced secretion without affecting baseline secretion. If the cells are exposed simultaneously to forskolin and OAG, but not 8-bromo-cAMP and OAG, the augmentation is dampened. This preliminary result suggests a possible interaction between protein kinase C and cAMP-dependent protein kinase in LH secretion regulation. We conclude that, regarding initiation of LH release, protein kinase C appears to be but one of a complex of mediators required for the secretory response to LHRH. Regarding the amplification of LHRH-induced release, activation of protein kinase C may be a component of the LHRH self-priming response.