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首页> 外文期刊>American Journal of Physiology >sgk: an essential convergence point for peptide and steroid hormone regulation of ENaC-mediated Na+ transport.
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sgk: an essential convergence point for peptide and steroid hormone regulation of ENaC-mediated Na+ transport.

机译：sgk：肽和类固醇激素调节ENaC介导的Na +转运的关键收敛点。

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摘要

To study the role of sgk (serum, glucocorticoid-induced kinase) in hormonal regulation of Na+ transport mediated by the epithelial Na+ channel (ENaC), clonal cell lines stably expressing human sgk, an S422A sgk mutant, or a D222A sgk mutant were created in the background of the A6 model renal epithelial cell line. Expression of normal sgk results in a 3.5-fold enhancement of basal transport and potentiation of the natriferic response to antidiuretic hormone (ADH). Transfection of a S422A mutant form of sgk, which cannot be phosphorylated by phosphatidylinositol-dependent kinase (PDK)-2, results in a cell line that is indistinguishable from the parent line in basal and hormone-stimulated Na+ transport. The D222A sgk mutant, which lacks kinase activity, functions as a dominant-negative mutant inhibiting basal as well as peptide- and steroid hormone-stimulated Na+ transport. Thus sgk activity is necessary for ENaC-mediated Na+ transport. Phosphorylation and activation by PDK-2 are necessary for sgk stimulation of ENaC. Expression of normal sgk over endogenous levels results in a potentiated natriferic response to ADH, suggesting that the enzyme is a rate-limiting step for the hormone response. In contrast, sgk does not appear to be the rate-limiting step for the cellular response to aldosterone or insulin.
机译：为了研究sgk（血清，糖皮质激素诱导的激酶）在激素调节上皮Na +通道（ENaC）介导的Na +转运中的作用，创建了稳定表达人sgk，S422A sgk突变体或D222A sgk突变体的克隆细胞系。在A6模型肾上皮细胞系的背景下。正常sgk的表达可导致基础转运增加3.5倍，并增强利尿剂对抗利尿激素（ADH）的应答。无法通过磷脂酰肌醇依赖性激酶（PDK）-2磷酸化的sgk的S422A突变体形式的转染，导致细胞系在基础和激素刺激的Na +转运中与亲本系没有区别。 D222A sgk突变体缺乏激酶活性，可作为显性阴性突变体，抑制基础以及肽和类固醇激素刺激的Na +转运。因此，sgk活性对于ENaC介导的Na +转运是必需的。 PDK-2的磷酸化和激活对于sgk刺激ENaC是必需的。正常sgk的表达超过内源水平会导致对ADH的强化钠铁反应，这表明该酶是激素反应的限速步骤。相反，sgk似乎不是细胞对醛固酮或胰岛素反应的限速步骤。

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