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首页> 外文期刊>Molecular and Cellular Endocrinology >Neurotensin enhances agonist-induced cAMP accumulation in PC3 cells via Ca2+ -dependent adenylyl cyclase(s).
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Neurotensin enhances agonist-induced cAMP accumulation in PC3 cells via Ca2+ -dependent adenylyl cyclase(s).

机译：神经降压素通过依赖Ca2 +的腺苷酸环化酶增强激动剂诱导的PC3细胞中cAMP的积累。

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摘要

A human prostate cancer cell line (PC3) with abundant neurotensin (NT) receptors was used to demonstrate that NT potentiated 3',5'-cyclic adenosine monophate (cAMP) accumulation in response to a variety of stimuli, including both direct forskolin (F) and indirect (prostaglandin, (PGE2), isoproterenol (ISO) and cholera toxin (CTx)) activators of adenylyl cyclase. Several mechanisms were investigated and our results indicated an effect on the rate of cAMP formation and not on degradation or extrusion. For each stimulus, NT enhanced efficacy without altering EC50. The effect of NT did not involve stimulatory G-protein (Gs)-activation or interference with a tonic inhibitory G-protein (Gi)-mediated inhibition. A similar response was obtained when NT was added with the stimulus or given as a two minute pulse which was removed prior to addition of stimulus. The potentiating activity disappeared with a t1,2 of approximately 15 min. NT transiently elevated cellular [Ca2+]i and its effects on cAMP could be mimicked by [Ca2+]i-elevating agents (uridine triphosphate (UTP), thapsigargin and ionomycin). Buffering cellular [Ca2+]i with 1,2-bis (2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester (BAPTA-AM) inhibited cAMP responses to ISO and F in presence and absence of NT. These data support the idea that NT potentiated cAMP formation in response to a variety of stimuli by facilitating the activation of Ca2+ -dependent adenylyl cyclases.
机译：具有丰富的神经降压素（NT）受体的人类前列腺癌细胞系（PC3）被用于证明NT能够响应多种刺激（包括直接福斯高林（F）在内的多种刺激来增强3'，5'-环腺苷一磷酸（cAMP）的积累）和腺苷酸环化酶的间接（前列腺素（PGE2），异丙肾上腺素（ISO）和霍乱毒素（CTx））激活剂。研究了几种机制，我们的结果表明对cAMP的形成速率有影响，而对降解或挤出没有影响。对于每种刺激，NT均能提高疗效而不会改变EC50。 NT的作用不涉及刺激性G蛋白（Gs）激活或对滋补性抑制性G蛋白（Gi）介导的抑制的干扰。当将NT与刺激物一起添加或以两分钟的脉冲形式给出时，获得相似的响应，在添加刺激物之前将其去除。增强活性以约15分钟的t1,2消失。 NT瞬时升高的细胞[Ca2 +] i及其对cAMP的作用可以通过[Ca2 +] i增强剂（三磷酸尿苷（UTP），毒胡萝卜素和离子霉素）来模仿。用1,2-双（2-氨基苯氧基）乙烷-N，N，N'，N'-四乙酸乙酰氧基甲基酯（BAPTA-AM）缓冲细胞[Ca2 +] i可以抑制cAMP对ISO和F的响应，无论是否存在新台币这些数据支持了NT通过促进Ca2 +依赖性腺苷酸环化酶的活化来增强cAMP响应各种刺激的想法。

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