Protein kinase C regulation of prolactin gene expression in lactotroph cells: involvement in dopamine inhibition.
Protein kinase C regulation of prolactin gene expression in lactotroph cells: involvement in dopamine inhibition.
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催乳素细胞中催乳素基因表达的蛋白激酶 C 调节：参与多巴胺抑制。
作者：
T. Chuang;L. Caccavelli;C. Kordon;A. Enjalbert
研究了蛋白激酶C(PKC)在多巴胺抑制原代培养的垂体前叶细胞PRL信使RNA(MRNA)水平中的作用。长期暴露于12-O-十四酰佛波醇13-乙酸酯(TPA)可使PKC脱敏。在TPA预处理后，短期(1-h)暴露于TPA不再能够触发PRL释放，证实了PKC脱敏的有效性。相反，非受体介导的促分泌剂与48 mM K+一起去极化释放激素的能力被保留下来。TPA预处理不影响基础PRL基因表达水平。相反，1 nM溴隐亭孵育4天后，可显著减轻1 nM溴隐亭对PRL mRNA的剂量依赖性抑制作用。由于多巴胺对PRL释放的抑制是通过cAMP、肌醇磷酸盐和钙离子等几个第二信使途径介导的，因此我们研究了PKC耗竭是否能够与这些途径的直接刺激相互作用。PKC可抑制Forskolin(FK)或8BrcAMP对PRL基因表达的刺激作用。同时，它也降低了基础水平和FK刺激的细胞内cAMP水平。此外，长期暴露于TPA可完全抑制硝苯地平对PRL mRNA的抑制作用，硝苯地平是一种二氢吡啶拮抗剂，可阻断电压依赖性钙通道。在相同条件下，TPA脱敏也影响溴隐亭、FK或硝苯地平对PRL释放的影响。这些结果表明，内源性PKC可以干扰cAMP和Ca~(2+)途径对催乳素基因表达的调节，这两个途径是与多巴胺作用有关的两个第二信使。
The role of protein kinase C (PKC) on dopamine inhibition of PRL messenger RNA (mRNA) levels was studied in anterior pituitary cells kept in primary culture. PKC was desensitized by long-term exposure to 12-O-tetradecanoylphorbol 13-acetate (TPA). Effectiveness of PKC desensitization was confirmed by the fact that after TPA pretreatment, short-term (1-h) exposure to TPA was no longer able to trigger PRL release. In contrast, the capacity of nonreceptor-mediated secretagogues as depolarization with 48 mM K+ to release the hormone was preserved. Pretreatment with TPA did not affect basal PRL mRNA levels. In contrast, it significantly reduced the dose-dependent inhibition of PRL mRNA induced by 1 nM bromocriptine after a 4-day incubation period. Since dopamine inhibition of PRL release is mediated by several second messager pathways, including cAMP, inositol phosphates, and Ca2+, we investigated whether PKC depletion was able to interact with direct stimulation of these pathways. Pretreatment with PKC suppressed stimulation of PRL mRNA levels induced by either Forskolin (FK) or 8Br-cAMP. In parallel, it reduced basal as well as FK stimulated intracellular cAMP levels. In addition, chronic exposure to TPA completely suppressed PRL mRNA inhibition induced by nifedipine, a dihydropyridine antagonist which blocks voltage-dependent Ca2+ channels. TPA desensitization also affected the action of bromocriptine, FK or nifedipine on PRL release measured under the same conditions. The data indicate that endogenous PKC can interfere with the regulation of PRL gene expression induced by both cAMP and Ca2+ pathways, two second messengers associated with the action of dopamine in lactotroph cells.
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促甲状腺激素释放激素发挥快速核效应，增加初级催乳素 mRNA 转录物的产生。
DOI：
10.1073/pnas.78.11.6662
发表时间：
1981
影响因子：
11.1
作者：
Potter,E;Nicolaisen,AK;Ong,ES;Evans,RM;Rosenfeld,MG
通讯作者：
Rosenfeld,MG
影响因子：
--
作者：
R. Day;R. Maurer
通讯作者：
R. Day;R. Maurer
催乳素和 c-fos mRNA 的钙诱导与蛋白激酶 C 活性无关。
DOI：
--
发表时间：
1989
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Bandyopadhyay,SK;Bancroft,C
通讯作者：
Bancroft,C
肿瘤促进剂增强垂体前叶细胞中基础和生长激素释放因子刺激的环AMP水平。
DOI：
10.1016/0006-291x(85)90165-2
发表时间：
1985
影响因子：
3.1
作者：
Cronin,MJ;Canonico,PL
通讯作者：
Canonico,PL
影响因子：
8
作者：
Kondo, T;Minamino, N;Tanaka, N
通讯作者：
Tanaka, N