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首页> 外文期刊>American Journal of Physiology >cAMP-stimulated Na+ transport in H441 distal lung epithelial cells: role of PKA, phosphatidylinositol 3-kinase, and sgk1.
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cAMP-stimulated Na+ transport in H441 distal lung epithelial cells: role of PKA, phosphatidylinositol 3-kinase, and sgk1.

机译：cAMP刺激的H441远端肺上皮细胞中的Na +转运：PKA，磷脂酰肌醇3激酶和sgk1的作用。

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摘要

H441 cells, a bronchiolar epithelial cell line, develop a cAMP-regulated benzamil-sensitive Na+ transport pathway on permeable supports (Itani OA, Auerbach SD, Husted RF, Volk KA, Ageloff S, Knepper MA, Stokes JB, Thomas CP. Am J Physiol Lung Cell Mol Physiol 282: L631-L641, 2002). To understand the molecular basis for the stimulation of Na+ transport, we delineated the role of specific intracellular pathways and examined the effect of cAMP on alphabetagamma-epithelial Na+ channel (ENaC) and sgk1 expression. Na+ transport increases within 5 min of cAMP stimulation and is sustained for >24 h. The sustained effect of cAMP on Na+ transport is abolished by LY-294002, an inhibitor of phosphatidylinositol 3-kinase, by H89, an inhibitor of PKA, or by SB-202190, an inhibitor of p38 MAP kinase. The sustained effect of cAMP was associated with increases in alpha-ENaC mRNA and protein but without a detectable increase in betagamma-ENaC and sgk1. The early effect of cAMP on Na+ transport is brefeldin sensitive andis mediated via PKA. These results are consistent with a model where the early effect of cAMP is to increase trafficking of Na+ channels to the apical cell surface whereas the sustained effect requires the synthesis of alpha-ENaC.
机译：H441细胞是一种细支气管上皮细胞系，在可渗透的支持物（Itani OA，Auerbach SD，Husted RF，Volk KA，Ageloff S，Knepper MA，Stokes JB，Thomas CP。Am J生理肺细胞分子生理学282：L631-L641，2002）。为了了解刺激Na +转运的分子基础，我们描述了特定细胞内途径的作用，并研究了cAMP对字母γ-上皮Na +通道（ENaC）和sgk1表达的影响。 Na +转运在cAMP刺激后5分钟内增加，并持续> 24小时。 cAMP对Na +转运的持续作用被磷脂酰肌醇3激酶抑制剂LY-294002，PKA抑制剂H89或p38 MAP激酶抑制剂SB-202190废除了。 cAMP的持续作用与α-ENaCmRNA和蛋白质的增加有关，但在betagamma-ENaC和sgk1中却没有可检测到的增加。 cAMP对Na +转运的早期作用是布雷菲尔丁敏感的，并且是通过PKA介导的。这些结果与模型相符，在模型中，cAMP的早期作用是增加Na +通道向根尖细胞表面的运输，而持续作用需要合成α-ENaC。

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