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首页> 外文期刊>American Journal of Physiology >Expression of rat Na-K-ATPase a2 enables ion pumping but not ouabain-induced signaling in a 1-deficient porcine renal epithelial cells
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Expression of rat Na-K-ATPase a2 enables ion pumping but not ouabain-induced signaling in a 1-deficient porcine renal epithelial cells

机译：大鼠Na-k-ATPase A2的表达使得在1缺陷的猪肾上皮细胞中能够离子泵送，但不是Oubain-诱导的信号传导

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Na-K-ATPase is a fundamental component of ion transport. Four a isoforms of the Na-K-ATPase catalytic a subunit are expressed in human cells. The ubiquitous Na-K-ATPase od was recently discovered to also mediate signal transduction through Src kinase. In contrast, ot2 expression is limited to a few cell types including myocytes, where it is coupled to the Na+/Ca2+ exchanger. To test whether rat Na-K-ATPase a.2 is capable of cellular signaling like its cd counterpart in a recipient mammalian system, we used anal knockdown pig renal epithelial cell (PY-17) to create an a2-expressing cell line with no detectable level of al expression. These cells exhibited normal ouabain-sensitive ATPase, but failed to effectively regulate Src. In contrast to cd-expressing cells, ouabain did not stimulate Src kinase or downstream effectors such as ERK and Akt in a2 cells, although their signaling apparatus was intact as evidenced by EGF-mediated signal transduction. Additionally, a.2 cells were unable to rescue caveolin-1. Unlike the NaKtide sequence derived from Na-K-ATPase al, which downregulates basal Src activity, the corresponding al NaKtide was unable to inhibit Src in vitro. Finally, coimmunoprecipi-tation of cellular Src was diminished in a2 cells. These findings indicate that Na-K-ATPase a2 does not regulate Src and, therefore, may not serve the same role in signal transduction as al. This further implies that the signaling mechanism of Na-K-ATPase is isoform specific, thereby supporting a model where al and a2 isoforms play distinct roles in mediating contraction and signaling in myocytes.
机译：Na-K-ATPase是离子运输的基本组分。 Na-K-ATP酶催化A亚基的四种同种型在人细胞中表达。最近发现普遍存在的Na-K-ATPase OD也通过SRC激酶介导信号转导。相反，OT2表达限于包括肌细胞的几种细胞类型，其中偶联至Na + / Ca2 +交换器。为了测试大鼠Na-k-ATPase A.2是否能够像受体哺乳动物系统中的CD对应物一样能够，我们使用肛门敲低猪肾上皮细胞（PY-17），以产生A2表达的细胞系没有可检测的Al表达水平。这些细胞表现出正常的Ouabain敏感的ATP酶，但未有效地调节SRC。与CD表达的细胞相反，Ouabain在A2细胞中没有刺激SRC激酶或下游效应（如ERK和AKT），尽管通过EGF介导的信号转导证明它们的信号传导装置完好无损。另外，A.2细胞不能拯救Caveolin-1。与从Na-K-ATPASE A1衍生的肿瘤序列不同，该肿瘤序列下调基础SRC活性，相应的Al肿瘤不能在体外抑制SRC。最后，在A2细胞中降低了细胞Src的Coimmunopropipi-Tative。这些发现表明Na-K-ATPase A2不调节SRC，因此，可能在信号转导中不能与Al中的相同作用。这进一步意味着Na-K-ATPase的信号传导机制是特异性的，从而支持Al和A2同种型在肌细胞中介导收缩和信号传导中具有不同作用的模型。

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