Modulation of adenylate cyclase/cyclic AMP response by thyrotropin and prostaglandin E2 in cultured thyroid cells. 1. Negative regulation.
Modulation of adenylate cyclase/cyclic AMP response by thyrotropin and prostaglandin E2 in cultured thyroid cells. 1. Negative regulation.
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促甲状腺素和前列腺素 E2 在培养的甲状腺细胞中调节腺苷酸环化酶/环 AMP 反应。
DOI：
10.1111/j.1432-1033.1978.tb12584.x
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发表时间：
1978
期刊：
影响因子：
--
通讯作者：
S. Lissitzky
中科院分区：
文献类型：
--
作者：
N. Takasu;B. Charrier;J. Mauchamp;S. Lissitzky
分离的猪甲状腺细胞，在促甲状腺素（大于或等于0.25 mU/ml）或前列腺素E2（大于或等于0.1微米）存在下培养，分别对进一步的促甲状腺素或前列腺素E2刺激显示腺苷3′：5′-单磷酸腺苷（环AMP）反应降低。对促甲状腺素和前列腺素E2的耐受性过程动力学不同：(a)对前列腺素E2的耐受性在暴露于前列腺素E2 2- 6小时后达到最大，而对促甲状腺素的耐受性仅在暴露于前列腺素E2 12- 24小时后达到最大；(b)前列腺素E2的难治程度远大于促甲状腺素。对促甲状腺激素或前列腺素E2的难治性的特点是：每种甲状腺刺激剂的特异性；依赖于促甲状腺素或前列腺素E2的剂量，例如，0.5 mU/ml促甲状腺素（或1微米前列腺素E2）诱导高度难治性，仅引起小的循环AMP增加；按时间要求归纳；局部效应；通过循环AMP响应的最大激活变化；可逆性。这种环AMP反应的难愈性不是由二丁基腺苷3':5'-单磷酸诱导的。这不是由于环amp -磷酸二酯酶活性的增加，而是由于受体-腺苷酸环化酶系统的改变。放线菌素D、嘌呤霉素和环己亚胺对促甲状腺素或前列腺素E2的耐受性的预防表明，需要新的RNA和蛋白质的合成来形成耐受性状态。
Isolated porcine thyroid cells, cultured in the presence of thyrotropin (greater than or equal to 0.25 mU/ml) or prostaglandin E2 (greater than or equal to 0.1 micron), showed decreased adenosine 3':5'-monophosphate (cyclic AMP) response to further thyrotropin or prostaglandin E2 stimulation, respectively. Kinetics of the refractory process to thyrotropin and prostaglandin E2 are different: (a) maximal refractoriness to prostaglandin E2 was attained after 2--6 h exposure to prostaglandin E2 while refractoriness to thyrotropin was maximal only after 12--24 h; (b) the degree of refractoriness to prostaglandin E2 was much greater than that to thyrotropin. Refractoriness to thyrotropin or prostaglandin E2 is characterized: by specificity for each thyroid stimulator; by dependence upon the dose of thyrotropin or prostaglandin E2 in culture, e.g. induction of high degree of refractoriness with 0.5 mU/ml thyrotropin (or 1 micron prostaglandin E2), which elicits only a small cyclic AMP increase; by time requirement for induction; by partial effect; by changes of maximum activation of cyclic AMP response; by reversibility. This refractoriness of the cyclic AMP response was not induced by dibutyryl adenosine 3':5'-monophosphate. It was not attributed to increased cyclic AMP-phosphodiesterase activity, but to alterations in the receptor-adenylate cyclase system. Prevention of refractoriness to thyrotropin or prostaglandin E2 by incubation of cells in the presence of actinomycin D, puromycin and cycloheximide suggests that new RNA and protein syntheses are required for the development of the refractory state.