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首页> 外文期刊>Life sciences >The cyclic AMP-dependent protein kinase A pathway is involved in progesterone effects on calcitonin secretion from TT cells
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The cyclic AMP-dependent protein kinase A pathway is involved in progesterone effects on calcitonin secretion from TT cells

机译：环AMP依赖性蛋白激酶A通路参与孕酮对TT细胞降钙素分泌的影响

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摘要

It is well known that gonadal steroid hormones influence the level of plasma calcitonin (CT), but the mechanism by which progesterone affects CT secretion is not clear. Immortalized TT cells are a reliable model system for studying the endocrine function of human parafollicular cells. In the present study, the effects of progesterone on CT secretion were examined in TT cells. TT cells were incubated in medium containing vehicle (DMSO), progesterone or BSA-progesterone for 60 or 150 min, and then the levels of CT in the medium, progesterone receptors, cAMP accumulation and CT mRNA expression were measured. To study the correlation between progesterone effects and the cAMP-dependent protein kinase A (PKA) pathway, cell lysates or cells in 24-well plates were treated with either vehicle or progesterone plus RU486, SQ22536, KT5720, or 3-isobutyl-1 -methylxanthine. Then, adenylyl cyclase and protein kinase A (PKA) activities were measured in the cell lysates, and the CT levels were measured in the medium from the 24-well plate. The activated cAMP response element binding protein (P-CREB) was also measured by immunofluorescence. Administration of 1 mu M progesterone or 500 nM BSA-progesterone increased the secretion of CT by 381% and 100%, respectively. Progesterone receptors A and B were downregulated by progesterone treatment. The cAMP concentration, adenylyl cyclase and PKA activity, CT mRNA expression, and nuclear P-CREB concentrations all showed an increase after progesterone treatment. RU486, SQ22536 and KT5720 inhibited the progesterone-stimulated effects. These results suggest that a cAMP-dependent PKA pathway is involved in progesterone-stimulated effects on CT secretion from TT cells. (c) 2007 Elsevier Inc. All rights reserved.
机译：众所周知，性腺类固醇激素会影响血浆降钙素（CT）的水平，但孕酮影响CT分泌的机制尚不清楚。永生化的TT细胞是用于研究人滤泡旁细胞内分泌功能的可靠模型系统。在本研究中，在TT细胞中检查了孕酮对CT分泌的影响。将TT细胞在含有媒介物（DMSO），孕酮或BSA-孕酮的培养基中孵育60或150分钟，然后测量培养基中的CT水平，孕酮受体，cAMP蓄积和CT mRNA表达。为了研究孕酮作用与cAMP依赖性蛋白激酶A（PKA）途径之间的相关性，用溶媒或孕酮加RU486，SQ22536，KT5720或3-异丁基-1-处理24孔板中的细胞裂解物或细胞。甲基黄嘌呤。然后，在细胞裂解物中测量腺苷酸环化酶和蛋白激酶A（PKA）的活性，并在24孔板的培养基中测量CT的水平。活化的cAMP反应元件结合蛋白（P-CREB）也通过免疫荧光测定。施用1μM的孕酮或500 nM的BSA-孕酮分别使CT的分泌增加381％和100％。孕酮治疗下调了孕酮受体A和B。孕酮治疗后，cAMP浓度，腺苷酸环化酶和PKA活性，CT mRNA表达以及核P-CREB浓度均增加。 RU486，SQ22536和KT5720抑制了孕激素刺激的作用。这些结果表明，依赖cAMP的PKA途径参与了孕酮对TT细胞CT分泌的刺激作用。 （c）2007 Elsevier Inc.保留所有权利。

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