Handwerger S, Harman I, Costello A, Markoff E
Mol Cell Endocrinol. 1987 Mar;50(1-2):99-106. doi: 10.1016/0303-7207(87)90081-5.
Exposure of human decidual cells for 0.5 h to dibutyryl cAMP, isobutyl-methylxanthine (IBMX), cholera toxin or forskolin caused a dose-dependent inhibition of prolactin release with maximal inhibition by each agent of 50-60%. Dibutyryl cAMP (5 mM), IBMX (0.5 mM), and cholera toxin (10 micrograms/ml) also inhibited prolactin synthesis to the same extent as prolactin release. Dibutyryl cAMP, IBMX, and cholera toxin, however, had no effect on the release of 35S-methionyl-prolactin from decidual cells preincubated for 24 h in medium with 35S-methionine. These agents, however, had no effects on the synthesis or release of TCA-precipitable 35S-decidual proteins and did not cause the degradation of intracellular or released prolactin. The demonstration that agents which increase intracellular cAMP levels inhibit the synthesis and release of decidual prolactin strongly implicates cAMP as a second messenger in the regulation of the synthesis and release of the hormone. The inhibitory effect of cAMP on prolactin release appears to be on the release from a rapidly releasable, newly synthesized intracellular prolactin pool.
将人蜕膜细胞暴露于二丁酰环磷腺苷(dibutyryl cAMP)、异丁基甲基黄嘌呤(IBMX)、霍乱毒素或福斯高林(forskolin)0.5小时,会导致催乳素释放呈剂量依赖性抑制,每种试剂的最大抑制率为50 - 60%。二丁酰环磷腺苷(5 mM)、异丁基甲基黄嘌呤(0.5 mM)和霍乱毒素(10微克/毫升)对催乳素合成的抑制程度与催乳素释放相同。然而,二丁酰环磷腺苷、异丁基甲基黄嘌呤和霍乱毒素对在含35S - 甲硫氨酸的培养基中预孵育24小时的蜕膜细胞释放35S - 甲硫氨酰 - 催乳素没有影响。然而,这些试剂对三氯乙酸(TCA)沉淀的35S - 蜕膜蛋白的合成或释放没有影响,也不会导致细胞内或释放的催乳素降解。增加细胞内cAMP水平的试剂会抑制蜕膜催乳素的合成和释放,这一证明有力地表明cAMP作为第二信使参与了该激素合成和释放的调节。cAMP对催乳素释放的抑制作用似乎作用于从快速可释放的、新合成的细胞内催乳素池中释放。