ArticleMolecular pharmacology2012
Sustained activation of N-methyl-D-aspartate receptors in podoctyes leads to oxidative stress, mobilization of transient receptor potential canonical 6 channels, nuclear factor of activated T cells activation, and apoptotic cell death.
Article in Molecular pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 52 citations in OpenAlex.
- Nicotinism vs. Glomerulopathies-Smoking as a Risk Factor for Primary Glomerulopathies.Antioxidants (Basel, Switzerland) · 2025Review
- The roles of TRPC6 in renal tubular disorders: a narrative review.Renal failure · 2024Review
- Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024Review
- Mitochondrial Signaling, the Mechanisms of AKI-to-CKD Transition and Potential Treatment Targets.International journal of molecular sciences · 2024Review
- Store-operated CaExperimental biology and medicine (Maywood, N.J.) · 2023Review
- The characteristics of extrachromosomal circular DNA in patients with end-stage renal disease.European journal of medical research · 2023Article
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- The Effects of TRPC6 Knockout in Animal Models of Kidney Disease.Biomolecules · 2022Review
- Gastrointestinal motility modulation by stress is associated with reduced smooth muscle contraction through specific transient receptor potential channel.The Journal of veterinary medical science · 2021Article
- NMDA receptor-mediated CaMKII/ERK activation contributes to renal fibrosis.BMC nephrology · 2020Article
- Glutamate-Gated NMDA Receptors: Insights into the Function and Signaling in the Kidney.Biomolecules · 2020Review
- Transmembrane insertases andThe Journal of biological chemistry · 2019Article
- Hydrogen sulfide inhibits CaAmerican journal of physiology. Endocrinology and metabolism · 2019Article
- Expression of Glutamate Receptor Subtype 3 Is Epigenetically Regulated in Podocytes under Diabetic Conditions.Kidney diseases (Basel, Switzerland) · 2019Article
- TRPC5 Does Not Cause or Aggravate Glomerular Disease.Journal of the American Society of Nephrology : JASN · 2018Article
- Estradiol mitigates ischemia reperfusion-induced acute renal failure through NMDA receptor antagonism in rats.Molecular and cellular biochemistry · 2017Article
- TRPC3 Channels in Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2017Review
- Article
- 20-Hydroxyeicosatetraenoic Acid (20-HETE) Modulates Canonical Transient Receptor Potential-6 (TRPC6) Channels in Podocytes.Frontiers in physiology · 2016Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Atypical N-methyl-D-aspartate (NMDA) receptors are expressed in podocytes. Sustained (≥24 h) application of 50 to100 μM NMDA to immortalized mouse podocytes evoked a marked increase in the production of reactive oxygen species(ROS) such as H₂O₂. This effect of NMDA was associated with increased cell-surface expression of p47(phox), a cytosolic regulatory subunit of the NADPH oxidase NOX2. NMDA-evoked generation of ROS drove an increase in steady-state surface expression of transient receptor potential canonical (TRPC) 6 channels, which was blocked by the NMDA antagonist dizocilpine(MK-801) and by a membrane-permeable scavenger of ROS. The effect of NMDA on TRPC6 was observed using cell surface biotinylation assays and also with whole-cell recordings made under conditions designed to facilitate detection of current through TRPC6. NMDA mobilization of TRPC6 channels was blocked by concurrent treatment with the NMDA antagonist MK-801 and by a membrane-permeable scavenger ofROS. Mobilization of TRPC6 was also evoked by L-homocysteic acid. NMDA treatment also increased nuclear localization of endogenous nuclear factor of activated T cells, which could be blocked by MK-801, by scavenging ROS, by the calcineurin inhibitor cyclosporine, and by the TRPC channel inhibitor 1-[2-(4-methoxyphenyl)-2-[3-(4-methoxyphenyl)propoxy]ethyl]imidazole (SKF-96365). NMDA treatment also evoked robust activation of Rho but not Rac,consistent with previous studies of downstream effectors of TRPC6 activation. Exposing cells to NMDA for 24 h reduced total and cell surface expression of the podocyte markers nephrin and podocin, but there was no loss of cells. With longer NMDA exposure (72 h), we observed loss of cells associated with nuclear fragmentation and increased expression of caspase-3, caspase-6, and Bax, suggesting an apoptotic process.
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