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Sodium transport is modulated by p38 kinase-dependent cross-talk between ENaC and Na,K-ATPase in collecting duct principal cells

Wang, Yu-Bao
Maunsbach, Arvid B
Doucet, Alain
Dizin, Eva
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Published in Journal of the American Society of Nephrology. 2014, vol. 25, no. 2, p. 250-259
Abstract In relation to dietary Na(+) intake and aldosterone levels, collecting duct principal cells are exposed to large variations in Na(+) transport. In these cells, Na(+) crosses the apical membrane via epithelial Na(+) channels (ENaC) and is extruded into the interstitium by Na,K-ATPase. The activity of ENaC and Na,K-ATPase must be highly coordinated to accommodate variations in Na(+) transport and minimize fluctuations in intracellular Na(+) concentration. We hypothesized that, independent of hormonal stimulus, cross-talk between ENaC and Na,K-ATPase coordinates Na(+) transport across apical and basolateral membranes. By varying Na(+) intake in aldosterone-clamped rats and overexpressing γ-ENaC or modulating apical Na(+) availability in cultured mouse collecting duct cells, enhanced apical Na(+) entry invariably led to increased basolateral Na,K-ATPase expression and activity. In cultured collecting duct cells, enhanced apical Na(+) entry increased the basolateral cell surface expression of Na,K-ATPase by inhibiting p38 kinase-mediated endocytosis of Na,K-ATPase. Our results reveal a new role for p38 kinase in mediating cross-talk between apical Na(+) entry via ENaC and its basolateral exit via Na,K-ATPase, which may allow principal cells to maintain intracellular Na(+) concentrations within narrow limits.
Keywords AMP-Activated Protein Kinases/physiologyAldosterone/physiologyAnimalsBasement Membrane/metabolismBiological Transport, Active/physiologyCell Line, TransformedCell Membrane/metabolismCell PolarityEndocytosis/physiologyEnzyme InductionEpithelial Sodium Channels/biosynthesis/genetics/physiologyHomeostasis/physiologyIntracellular Fluid/metabolismIon Transport/physiologyKidney Tubules, Collecting/cytology/metabolismLysosomes/metabolismMAP Kinase Signaling System/drug effects/physiologyMaleMiceRatsRats, Sprague-DawleySodium/metabolismSodium-Potassium-Exchanging ATPase/biosynthesis/genetics/metabolism/physiologyp38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/physiology
PMID: 24179170
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Research group Laboratoire de physiologie et pathophysiologie des cellules rénales (29)
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WANG, Yu-Bao et al. Sodium transport is modulated by p38 kinase-dependent cross-talk between ENaC and Na,K-ATPase in collecting duct principal cells. In: Journal of the American Society of Nephrology, 2014, vol. 25, n° 2, p. 250-259. doi: 10.1681/ASN.2013040429 https://archive-ouverte.unige.ch/unige:89617

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Deposited on : 2016-11-30

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