ArticleJournal of the American Society of Nephrology : JASN2014
Sodium transport is modulated by p38 kinase-dependent cross-talk between ENaC and Na,K-ATPase in collecting duct principal cells.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Intracellular CaiScience · 2024Article
- Cingulin and paracingulin tether myosins-2 to junctions to mechanoregulate the plasma membrane.The Journal of cell biology · 2023Article
- Review
- Emerging roles of proximal tubular endocytosis in renal fibrosis.Frontiers in cell and developmental biology · 2023Review
- Cingulin binds to the ZU5 domain of scaffolding protein ZO-1 to promote its extended conformation, stabilization, and tight junction accumulation.The Journal of biological chemistry · 2022Article
- The role of AMPK in regulation of NaJournal of muscle research and cell motility · 2021Review
- Interaction between Epithelial Sodium ChannelJournal of the American Society of Nephrology : JASN · 2020Article
- The TNF-derived TIP peptide activates the epithelial sodium channel and ameliorates experimental nephrotoxic serum nephritis.Kidney international · 2019Article
- Impairment of Membrane Repolarization Accompanies Axon Transport Deficits in Glaucoma.Frontiers in neuroscience · 2019Article
- Dietary sodium induces a redistribution of the tubular metabolic workload.The Journal of physiology · 2017Article
- Effects of gonadectomy and testosterone treatment on aquaporin expression in the kidney of normotensive and hypertensive rats.Experimental biology and medicine (Maywood, N.J.) · 2017Article
- Coordinated Control of ENaC and Na+,K+-ATPase in Renal Collecting Duct.Journal of the American Society of Nephrology : JASN · 2016Review
- The mineralocorticoid receptor (MR) regulates ENaC but not NCC in mice with random MR deletion.Pflugers Archiv : European journal of physiology · 2016Article
- Downregulation of Organic Anion Transporting Polypeptide (OATP) 1B1 Transport Function by Lysosomotropic Drug Chloroquine: Implication in OATP-Mediated Drug-Drug Interactions.Molecular pharmaceutics · 2016Article
- CPT-cGMP Is A New Ligand of Epithelial Sodium Channels.International journal of biological sciences · 2016Review
- Urinary serine proteases and activation of ENaC in kidney--implications for physiological renal salt handling and hypertensive disorders with albuminuria.Pflugers Archiv : European journal of physiology · 2015Review
- Transcriptional regulators of Na,K-ATPase subunits.Frontiers in cell and developmental biology · 2015Review
- Binding of FGF2 to FGFR2 in an autocrine mode in trophectoderm cells is indispensable for mouse blastocyst formation through PKC-p38 pathway.Cell cycle (Georgetown, Tex.) · 2015Article
- Article
- Paradoxical activation of the sodium chloride cotransporter (NCC) without hypertension in kidney deficient in a regulatory subunit of Na,K-ATPase, FXYD2.Physiological reports · 2014Article
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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