Cyclic GMP may serve as a second messenger in peptide-induced muscle degeneration in an insect.
Cyclic GMP may serve as a second messenger in peptide-induced muscle degeneration in an insect.
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环状 GMP 可能作为昆虫肽诱导肌肉变性的第二信使。
DOI：
10.1073/pnas.81.21.6718
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发表时间：
1984
影响因子：
11.1
通讯作者：
Truman,JW
中科院分区：
文献类型：
--
作者：
Schwartz,LM;Truman,JW
在变态的末期，Antheraea Polyphemus的节间肌肉在多肽羽化激素的响应下经历快速退化。肌肉死亡之前，肌肉中的鸟苷-3‘，5’-环一磷酸(CGMP)滴度增加了22倍，在多肽暴露60分钟后达到峰值，而腺苷-3‘5’-环磷酸(CAMP)滴度保持不变。EH诱导肌肉cGMP含量呈剂量依赖性增加，其阈值剂量与诱导细胞死亡所需的剂量相似。外源性cGMP可模拟EH的作用，但cAMP不能。鸟苷环化酶激动剂硝普钠和3‘，5’-环核苷酸磷酸二酯酶抑制剂甲基化黄嘌呤也诱导了这些肌肉的选择性死亡。结论：cGMP水平升高参与了EH诱导的肌肉退行性变。在成体发育的末期，节间肌肉对EH变得敏感，这是对类固醇蜕皮激素滴度下降的反应。在早期，用EH、外源性cGMP、硝普钠或甲基化黄嘌呤治疗在导致细胞死亡方面无效。然而，此时使用EH治疗导致节段间肌肉cGMP显著增加。因此，对多肽激素的生理反应的开始可能是由于EH受体和鸟苷环化酶远端的生化变化。
At the end of metamorphosis, the intersegmental muscles of the moth Antheraea polyphemus undergo rapid degeneration in response to the peptide eclosion hormone (EH). Muscle death was preceded by a 22-fold increase in muscle guanosine-3',5'-cyclic monophosphate (cGMP) titers, which peaked 60 min after peptide exposure; adenosine-3'5'-cyclic monophosphate (cAMP) titers remained unchanged. EH induced a dose-dependent increase in muscle cGMP content with a threshold dose similar to that needed to induce cell death. Exogenous cGMP, but not cAMP, mimicked the action of EH. Sodium nitroprusside, a potent stimulator of guanylate cyclase, and methylated xanthines, a class of 3',5'-cyclic-nucleotide phosphodiesterase inhibitors, also induced the selective death of these muscles. It is concluded that an elevation of cGMP level is involved in EH-induced muscle degeneration. The intersegmental muscles become sensitive to EH at the end of adult development in response to the declining titers of the steroid molting hormones, the ecdysteroids. At earlier times, treatment with EH, exogenous cGMP, sodium nitroprusside, or methylated xanthines was ineffective in causing cell death. Nevertheless, treatment with EH at this time resulted in a marked increase in intersegmental-muscle cGMP. Thus, the onset of physiological responsiveness to the peptide hormone presumably results from biochemical changes distal to the EH receptors and guanylate cyclase.