Investigation of presumptive mobilization pathways for calcium in the steroidogenic action of big prothoracicotropic hormone.
Investigation of presumptive mobilization pathways for calcium in the steroidogenic action of big prothoracicotropic hormone.
复制标题
大促胸腺激素类固醇生成作用中钙的假定动员途径的研究。
DOI：
10.1016/0965-1748(96)00001-x
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发表时间：
1996
影响因子：
3.8
通讯作者：
Smith,WA
中科院分区：
文献类型：
--
作者：
Girgenrath,S;Smith,WA
烟草天蛾 Manduca sexta 前胸腺的蜕皮类固醇生成受到脑神经肽促前胸腺激素 (PTTH) 的刺激。 PTTH 刺激的 cAMP 合成和蜕皮激素分泌依赖于细胞外钙的存在，表明 PTTH 增强钙进入细胞质。这种进入细胞质的过程可能涉及质膜钙通道的打开，或者依赖于先前肌醇三磷酸（IP3）介导的细胞内储存的钙的释放的机制。在蛹前胸腺中，即使存在锂，PTTH 也不会在数秒至 30 分钟的时间内增加 IP3 或其他肌醇磷酸盐。然而，L型钙通道拮抗剂尼群地平完全阻止PTTH刺激的蜕皮激素合成。前胸腺中的 41 kDa G 蛋白被百日咳毒素 ADP 核糖基化。然而，PTTH 刺激的蜕皮激素合成不受先前暴露于百日咳毒素的影响，表明 41 kDa 蛋白不参与类固醇生成的急性刺激。相比之下，霍乱毒素对蜕皮激素分泌有刺激作用，表明 Gs 样蛋白参与其中。基于蛹前胸腺中不存在 PTTH 刺激的磷酸肌醇形成，表明钙动员可能通过钙通道的开放发生，可能受 Gs 调节。
Ecdysteroidogenesis in the prothoracic glands of the tobacco hornworm Manduca sexta is stimulated by the cerebral neuropeptide prothoracicotropic hormone (PTTH). PTTH-stimulated cAMP synthesis and ecdysone secretion are dependent on the presence of extracellular calcium, suggesting that PTTH enhances calcium entry into the cytosol. Such entry into the cytosol might involve the opening of a plasma membrane calcium channel, or a mechanism dependent upon prior inositol triphosphate (IP3)-mediated release of intracellularly stored calcium. In pupal prothoracic glands, PTTH does not increase IP3or other inositol phosphates over times ranging from seconds up to 30 min, even in the presence of lithium. However, the L-type calcium channel antagonist nitrendipine completely prevents PTTH-stimulated ecdysone synthesis. A 41 kDa G-protein in prothoracic glands is ADP-ribosylated by pertussis toxin. However, PTTH-stimulated ecdysone synthesis is unaffected by prior exposure to pertussis toxin, indicating that the 41 kDa protein is not involved in the acute stimulation of steroidogenesis. By contrast, cholera toxin has a stimulatory effect on ecdysone secretion suggesting the involvement of a Gs-like protein. Based on the absence of PTTH-stimulated inositol phosphate formation in pupal prothoracic glands, it is suggested that calcium mobilization may occur through the opening of a calcium channel, possibly regulated by Gs.