ArticleAmerican journal of physiology. Renal physiology2014
ATP acting through P2Y receptors causes activation of podocyte TRPC6 channels: role of podocin and reactive oxygen species.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 64 citations in OpenAlex.
- Preclinical approaches to studying liver and kidney fibrosis: models and methodologies.Frontiers in pharmacology · 2026Review
- TRPC6 effects on albumin permeation, nephrin shedding, and apoptosis in podocytes: Role of calcineurin and metalloproteases.Physiological reports · 2025Article
- The roles of TRPC6 in renal tubular disorders: a narrative review.Renal failure · 2024Review
- Renin-angiotensin system-mediated nitric oxide signaling in podocytes.American journal of physiology. Renal physiology · 2024Article
- Calcium signalling and transport in the kidney.Nature reviews. Nephrology · 2024Review
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- The Effects of TRPC6 Knockout in Animal Models of Kidney Disease.Biomolecules · 2022Review
- Article
- Pannexin 1: a novel regulator of acute hypoxic pulmonary vasoconstriction.Cardiovascular research · 2022Article
- TRPC6 Inactivation Reduces Albuminuria Induced by Protein Overload in Sprague Dawley Rats.Cells · 2022Article
- Article
- Potential Therapeutic Targets of Rehmannia Formulations on Diabetic Nephropathy: A Comparative Network Pharmacology Analysis.Frontiers in pharmacology · 2022Article
- Reno-Protective Effect of GLP-1 Receptor Agonists in Type1 Diabetes: Dual Action on TRPC6 and NADPH Oxidases.Biomedicines · 2021Article
- Characterization of purinergic receptor 2 signaling in podocytes from diabetic kidneys.iScience · 2021Article
- Role of opioid signaling in kidney damage during the development of salt-induced hypertension.Life science alliance · 2020Article
- Pathogenesis and Damage Targets of Hypertensive Kidney Injury.Journal of translational internal medicine · 2020Article
- Review
- New insight into podocyte slit diaphragm, a therapeutic target of proteinuria.Clinical and experimental nephrology · 2020Review
- Extracellular Nucleotides and P2 Receptors in Renal Function.Physiological reviews · 2020Review
- TRPC Channels in Proteinuric Kidney Diseases.Cells · 2019Review
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Extracellular ATP may contribute to Ca(2+) signaling in podocytes during tubuloglomerular feedback (TGF) and possibly as a result of local tissue damage. TRPC6 channels are Ca(2+)-permeable cationic channels that have been implicated in the pathophysiology of podocyte diseases. Here we show using whole cell recordings that ATP evokes robust activation of TRPC6 channels in mouse podocyte cell lines and in rat podocytes attached to glomerular capillaries in ex vivo glomerular explants. The EC50 for ATP is ~10 μM and is maximal at 100 μM, and currents were blocked by the P2 antagonist suramin. In terms of maximal currents that can be evoked, ATP is the strongest activator of podocyte TRPC6 that we have characterized to date. Smaller currents were observed in response to ADP, UTP, and UDP. ATP-evoked currents in podocytes were abolished by TRPC6 knockdown and by pretreatment with 10 μM SKF-96365 or 50 μM La(3+). ATP effects were also abolished by inhibiting G protein signaling and by the PLC/PLA2 inhibitor D-609. ATP effects on TRPC6 were also suppressed by knockdown of the slit diaphragm scaffolding protein podocin, and also by tempol, a membrane-permeable quencher of reactive oxygen species. Modulation of podocyte TRPC6 channels, especially in foot processes, could provide a mechanism for regulation of glomerular function by extracellular nucleotides, possibly leading to changes in permeation through slit diaphragms. These results raise the possibility that sustained ATP signaling could contribute to foot process effacement, Ca(2+)-dependent changes in gene expression, and/or detachment of podocytes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.