Insulin desensitized beta 1-adrenergic receptor-mediated stimulation of adenylyl cyclase in SK-N-MC cells.
Insulin desensitized beta 1-adrenergic receptor-mediated stimulation of adenylyl cyclase in SK-N-MC cells.
复制标题
胰岛素使 SK-N-MC 细胞中 β1-肾上腺素能受体介导的腺苷酸环化酶刺激脱敏。
DOI：
10.1016/0024-3205(92)90164-k
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发表时间：
1992
期刊：
影响因子：
6.1
通讯作者：
Lopez,S
中科院分区：
文献类型：
--
作者：
Bahouth,SW;Lopez,S
受体串扰是一个新兴的领域，研究不同类别的受体之间的交叉调节。在本工作中，我们研究了激活胰岛素受体（酪氨酸激酶受体）对腺苷酸环化酶β激动剂激活的影响，腺苷酸环化酶β激动剂激活由G蛋白连接受体介导。用胰岛素处理SK INF 4 NMC神经上皮瘤细胞可显著减弱β1-肾上腺素能受体介导的腺苷酸环化酶刺激。这种效应需要纳摩尔浓度的胰岛素，在这些细胞暴露于胰岛素的几分钟内发生，并且不是由β-肾上腺素能受体的下调引起的。单独使用胰岛素可使异丙肾上腺素介导的腺苷酸环化酶刺激最大值降低50%，而同时加入磷酸酶抑制剂钒酸钠可使胰岛素抑制作用的幅度增加至90%。胰岛素为β-肾上腺素能受体及其跨膜信号通路的异源脱敏提供了另一种途径。
Receptor cross-talk is an emerging field which investigates cross-regulation between distinct classes of receptors. In the present work, we investigated the influence of activating the insulin receptor, a tyrosine kinase receptor, on β-agonist activation of adenylyl cyclase, which is mediated by a G protein-linked receptor. Treatment of SKNMC neuroepithelioma cells with insulin generated a marked attenuation of β1-adrenergic receptor-mediated stimulation of adenylyl cyclase. This effect required nanomolar concentrations of insulin, occured within minutes of exposure of these cells to insulin, and did not result from down-regulation of β-adrenergic receptors. Insulin alone reduced the maximal isoproterenol-mediated stimulation of adenylyl cyclase by 50%, while the co-addition of the phosphatase inhibitor sodium vanadate increased the magnitude of insulin inhibition to 90%. Insulin provides an additional avenue for heterologous desensitization of β-adrenergic receptors and their transmembranal signalling pathway.