ArticleJournal of molecular and cellular cardiology2013
Localization of sodium channel subtypes in mouse ventricular myocytes using quantitative immunocytochemistry.
Article in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 69 citations in OpenAlex.
- Late IMedicinal research reviews · 2026Review
- Selective activation of tetrodotoxin-sensitive sodium channels by AaH-II drives arrhythmogenic late Na+ current in the heart.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026Article
- Ion channels and cardiac disease: mechanisms and functions of a disintegrin and metalloproteases and their substrates.Frontiers in cell and developmental biology · 2026Review
- Hypernatremia Enhances Transient Outward Potassium and Late Sodium Currents in a Mouse Model of Long QT Syndrome Type 3.bioRxiv : the preprint server for biology · 2025Article
- SCN10A-short gene therapy to restore conduction and protect against malignant cardiac arrhythmias.European heart journal · 2025Article
- Voltage-gated sodium channels in excitable cells as drug targets.Nature reviews. Drug discovery · 2025Review
- Evaluating computational efforts and physiological resolution of mathematical models of cardiac tissue.Scientific reports · 2024Article
- Sodium channel subpopulations with distinct biophysical properties and subcellular localization enhance cardiac conduction.The Journal of general physiology · 2023Article
- Gene mutations in comorbidity of epilepsy and arrhythmia.Journal of neurology · 2023Review
- Absolute Quantification of Nav1.5 Expression by Targeted Mass Spectrometry.International journal of molecular sciences · 2022Article
- Late Sodium Current of the Heart: Where Do We Stand and Where Are We Going?Pharmaceuticals (Basel, Switzerland) · 2022Review
- Hypernatremia and intercalated disc edema synergistically exacerbate long-QT syndrome type 3 phenotype.American journal of physiology. Heart and circulatory physiology · 2021Article
- Ventricular voltage-gated ion channels: Detection, characteristics, mechanisms, and drug safety evaluation.Clinical and translational medicine · 2021Review
- IL-33 Is Involved in the Anti-Inflammatory Effects of Butyrate and Propionate on TNFα-Activated Endothelial Cells.International journal of molecular sciences · 2021Article
- miR-125 family regulates XIRP1 and FIH in response to myocardial infarction.Physiological genomics · 2020Article
- Regional differences in the expression of tetrodotoxin-sensitive inward CaChannels (Austin, Tex.) · 2019Article
- Properties of cardiac conduction in a cell-based computational model.PLoS computational biology · 2019Article
- Modeling Depolarization Delay, Sodium Currents, and Electrical Potentials in Cardiac Transverse Tubules.Frontiers in physiology · 2019Article
- A Distinct Pool of NaFrontiers in physiology · 2019Article
- Channelopathy as a SUDEP Biomarker in Dravet Syndrome Patient-Derived Cardiac Myocytes.Stem cell reports · 2018Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Voltage-gated sodium channels are responsible for the rising phase of the action potential in cardiac muscle. Previously, both TTX-sensitive neuronal sodium channels (NaV1.1, NaV1.2, NaV1.3, NaV1.4 and NaV1.6) and the TTX-resistant cardiac sodium channel (NaV1.5) have been detected in cardiac myocytes, but relative levels of protein expression of the isoforms were not determined. Using a quantitative approach, we analyzed z-series of confocal microscopy images from individual mouse myocytes stained with either anti-NaV1.1, anti-NaV1.2, anti-NaV1.3, anti-NaV1.4, anti-NaV1.5, or anti-NaV1.6 antibodies and calculated the relative intensity of staining for these sodium channel isoforms. Our results indicate that the TTX-sensitive channels represented approximately 23% of the total channels, whereas the TTX-resistant NaV1.5 channel represented 77% of the total channel staining in mouse ventricular myocytes. These ratios are consistent with previous electrophysiological studies in mouse ventricular myocytes. NaV1.5 was located at the cell surface, with high density at the intercalated disc, but was absent from the transverse (t)-tubular system, suggesting that these channels support surface conduction and inter-myocyte transmission. Low-level cell surface staining of NaV1.4 and NaV1.6 channels suggest a minor role in surface excitation and conduction. Conversely, NaV1.1 and NaV1.3 channels are localized to the t-tubules and are likely to support t-tubular transmission of the action potential to the myocyte interior. This quantitative immunocytochemical approach for assessing sodium channel density and localization provides a more precise view of the relative importance and possible roles of these individual sodium channel protein isoforms in mouse ventricular myocytes and may be applicable to other species and cardiac tissue types.
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