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哇巴因刺激肾近端小管细胞钠钾 atp 酶和 nhe3 的转运调节。

Ouabain-stimulated trafficking regulation of the Na/K-ATPase and NHE3 in renal proximal tubule cells.

机构信息

Department of Medicine, University of Toledo College of Medicine, Toledo, OH 43614-2598, USA.

出版信息

Mol Cell Biochem. 2012 Aug;367(1-2):175-83. doi: 10.1007/s11010-012-1331-x. Epub 2012 May 23.

DOI:10.1007/s11010-012-1331-x
PMID:22618525
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3475650/
Abstract

We have demonstrated that ouabain regulates protein trafficking of the Na/K-ATPase α1 subunit and NHE3 (Na/H exchanger, isoform 3) via ouabain-activated Na/K-ATPase signaling in porcine LLC-PK1 cells. To investigate whether this mechanism is species-specific, ouabain-induced regulation of the α1 subunit and NHE3 as well as transcellular (22)Na(+) transport were compared in three renal proximal tubular cell lines (human HK-2, porcine LLC-PK1, and AAC-19 originated from LLC-PK1 in which the pig α1 was replaced by ouabain-resistant rat α1). Ouabain-induced inhibition of transcellular (22)Na(+) transport is due to an ouabain-induced redistribution of the α1 subunit and NHE3. In LLC-PK1 cells, ouabain also inhibited the endocytic recycling of internalized NHE3, but has no significant effect on recycling of endocytosed α1 subunit. These data indicated that the ouabain-induced redistribution of the α1 subunit and NHE3 is not a species-specific phenomenon, and ouabain-activated Na/K-ATPase signaling influences NHE3 regulation.

摘要

我们已经证明，哇巴因通过猪 LLC-PK1 细胞中哇巴因激活的 Na/K-ATP 酶信号调节 Na/K-ATP 酶 α1 亚基和 NHE3（Na/H 交换器，亚型 3）的蛋白转运。为了研究这种机制是否具有物种特异性，我们比较了三种肾近端管状细胞系（人 HK-2、猪 LLC-PK1 和 AAC-19，它们起源于 LLC-PK1，其中猪的α1 被哇巴因抗性大鼠的α1 取代）中哇巴因诱导的α1 亚基和 NHE3 以及细胞间（22）Na（+）转运的调节。哇巴因诱导的细胞间（22）Na（+）转运抑制是由于哇巴因诱导的α1 亚基和 NHE3 的重新分布。在 LLC-PK1 细胞中，哇巴因还抑制了内吞 NHE3 的内吞循环，但对内吞α1 亚基的循环没有显著影响。这些数据表明，哇巴因诱导的α1 亚基和 NHE3 的重新分布不是一种物种特异性现象，而哇巴因激活的 Na/K-ATP 酶信号影响 NHE3 的调节。

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