ArticleJournal of the American Society of Nephrology : JASN2015
Caveolin-1 Deficiency Inhibits the Basolateral K+ Channels in the Distal Convoluted Tubule and Impairs Renal K+ and Mg2+ Transport.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Caveolin-1 Stabilizes SERCA2 to Counteract Acute Kidney Injury via Suppression of CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Calcineurin inhibitors stimulate Kir4.1/Kir5.1 of the distal convoluted tubule to increase NaCl cotransporter.JCI insight · 2023Article
- Inwardly rectifying KAmerican journal of physiology. Cell physiology · 2022Review
- Molecular Basis, Diagnostic Challenges and Therapeutic Approaches of Bartter and Gitelman Syndromes: A Primer for Clinicians.International journal of molecular sciences · 2021Review
- Epoxyeicosatrienoic acid metabolites inhibit Kir4.1/Kir5.1 in the distal convoluted tubule.American journal of physiology. Renal physiology · 2020Article
- Inhibition of AT2R and Bradykinin Type II Receptor (BK2R) Compromises High KHypertension (Dallas, Tex. : 1979) · 2020Article
- Pathophysiological Role of Caveolae in Hypertension.Frontiers in medicine · 2019Review
- Norepinephrine-Induced Stimulation of Kir4.1/Kir5.1 Is Required for the Activation of NaCl Transporter in Distal Convoluted Tubule.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4.1 potassium channel.Kidney international · 2018Article
- Caveolin 1 Promotes Renal Water and Salt Reabsorption.Scientific reports · 2018Article
- Caveolin-1 in the Pathogenesis of Diabetic Nephropathy: Potential Therapeutic Target?Current diabetes reports · 2017Review
- Role and mechanisms of regulation of the basolateral KActa physiologica (Oxford, England) · 2017Review
- Basolateral Kir4.1 activity in the distal convoluted tubule regulates K secretion by determining NaCl cotransporter activity.Current opinion in nephrology and hypertension · 2016Review
- The expression, regulation, and function of Kir4.1 (Kcnj10) in the mammalian kidney.American journal of physiology. Renal physiology · 2016Review
- Caveolin-1 regulates corneal wound healing by modulating Kir4.1 activity.American journal of physiology. Cell physiology · 2016Article
- Disruption of KCNJ10 (Kir4.1) stimulates the expression of ENaC in the collecting duct.American journal of physiology. Renal physiology · 2016Article
- Vasopressin-induced stimulation of the Na(+)-activated K(+) channels is responsible for maintaining the basolateral K(+) conductance of the thick ascending limb (TAL) in EAST/SeSAME syndrome.Biochimica et biophysica acta · 2015Article
- KCNJ10 (Kir4.1) is expressed in the basolateral membrane of the cortical thick ascending limb.American journal of physiology. Renal physiology · 2015Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Kcnj10 encodes the inwardly rectifying K(+) channel Kir4.1 in the basolateral membrane of the distal convoluted tubule (DCT) and is activated by c-Src. However, the regulation and function of this K(+) channel are incompletely characterized. Here, patch-clamp experiments in Kcnj10-transfected HEK293 cells demonstrated that c-Src-induced stimulation of Kcnj10 requires coexpression of caveolin-1 (cav-1), and immunostaining showed expression of cav-1 in the basolateral membrane of parvalbumin-positive DCT. Patch-clamp experiments detected a 40-pS inwardly rectifying K(+) channel, a heterotetramer of Kir4.1/Kir5.1, in the basolateral membrane of the early DCT (DCT1) in both wild-type (WT) and cav-1-knockout (KO) mice. However, the activity of this basolateral 40-pS K(+) channel was lower in KO mice than in WT mice. Moreover, the K(+) reversal potential (an indication of membrane potential) was less negative in the DCT1 of KO mice than in the DCT1 of WT mice. Western blot analysis demonstrated that cav-1 deficiency decreased the expression of the Na(+)/Cl(-) cotransporter and Ste20-proline-alanine-rich kinase (SPAK) but increased the expression of epithelial Na(+) channel-α. Furthermore, the urinary excretion of Mg(2+) and K(+) was significantly higher in KO mice than in WT mice, and KO mice developed hypomagnesemia, hypocalcemia, and hypokalemia. We conclude that disruption of cav-1 decreases basolateral K(+) channel activity and depolarizes the cell membrane potential in the DCT1 at least in part by suppressing the stimulatory effect of c-Src on Kcnj10. Furthermore, the decrease in Kcnj10 and Na(+)/Cl(-) cotransporter expression induced by cav-1 deficiency may underlie the compromised renal transport of Mg(2+), Ca(2+), and K(+).
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