Stimulation of Na,K-ATPase by Low Potassium Is Dependent on Transferrin |
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Authors: | W?Yin G?Jiang K?Takeyasu Email author" target="_blank">X?ZhouEmail author |
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Institution: | (1) Department of Medicine, Uniformed Services University of the Health Sciences, 4301, Jones Bridge Rd, Bethesda, MD 20814, USA;(2) Department of Anatomy, Uniformed Services University of the Health Sciences, 4301, Jones Bridge Rd, Bethesda, MD 20814, USA;(3) Department of Natural Environment Sciences, Kyoto University, Kyoto, Japan |
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Abstract: | We took advantage of the fact that confluent MDCK cells can survive in a serum-free medium for several days to examine whether the upregulation of Na,K-ATPase by low K+ required serum. We found that serum was essential for low K+ to induce an increase in the cell surface Na,K-ATPase molecular number as quantified by ouabain binding assays. Further analyses identified that transferrin, not EGF or IGF-1, could simulate the effect of serum. Moreover, transferrin was also required for low-K+-induced increases in 1-subunit promoter activity, 1- and 1-subunit protein abundance of the Na,K-ATPase. In the presence of transferrin, low K+ enhanced cellular uptake of iron. Inhibition of intracellular iron activity by deferoxamine (40 µM) abrogated the effect of low K+ on the Na,K-ATPase. Like deferoxamine, catalase (100 U/ml) also ablated the effect of low K+. We conclude that stimulation of the Na,K-ATPase by low K+ is dependent on transferrin. The effect of transferrin is mediated by increased iron transport and reactive oxygen species activity. |
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Keywords: | Iron Reactive oxygen species MDCK cells |
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