ArticleAmerican journal of physiology. Heart and circulatory physiology2008
Molecular identity of the late sodium current in adult dog cardiomyocytes identified by Nav1.5 antisense inhibition.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- The sodium/glucose cotransporter 2 inhibitor empagliflozin is a pharmacological chaperone of cardiac NaAmerican journal of physiology. Heart and circulatory physiology · 2025Article
- NaInternational journal of molecular sciences · 2024Article
- Characterization of NaLife science alliance · 2024Article
- Microtubule plus-end tracking proteins: novel modulators of cardiac sodium channels and arrhythmogenesis.Cardiovascular research · 2023Article
- Spinal cord injury-mediated changes in electrophysiological properties of rat gastric nodose ganglion neurons.Experimental neurology · 2022Article
- The molecular mechanisms of MLKL-dependent and MLKL-independent necrosis.Journal of molecular cell biology · 2021Review
- Cardiac T-Tubule cBIN1-Microdomain, a Diagnostic Marker and Therapeutic Target of Heart Failure.International journal of molecular sciences · 2021Review
- Long QT syndrome - Bench to bedside.Heart rhythm O2 · 2021Article
- Drug Development and the Use of Induced Pluripotent Stem Cell-Derived Cardiomyocytes for Disease Modeling and Drug Toxicity Screening.International journal of molecular sciences · 2020Review
- Elevated ocular pressure reduces voltage-gated sodium channel NaV1.2 protein expression in retinal ganglion cell axons.Experimental eye research · 2020Article
- Phosphorylation of cardiac voltage-gated sodium channel: Potential players with multiple dimensions.Acta physiologica (Oxford, England) · 2019Review
- The functional consequences of sodium channel NaESC heart failure · 2019Article
- Transmural cellular heterogeneity in myocardial electromechanics.The journal of physiological sciences : JPS · 2018Article
- Intracellular trafficking pathways of Cx43 gap junction channels.Biochimica et biophysica acta. Biomembranes · 2018Review
- Basal late sodium current is a significant contributor to the duration of action potential of guinea pig ventricular myocytes.Physiological reports · 2017Article
- Cardiac T-Tubule Microanatomy and Function.Physiological reviews · 2017Review
- Biology of the cardiac myocyte in heart disease.Molecular biology of the cell · 2016Review
- BIN1 regulates dynamic t-tubule membrane.Biochimica et biophysica acta · 2016Review
- Cardiomyocyte protein trafficking: Relevance to heart disease and opportunities for therapeutic intervention.Trends in cardiovascular medicine · 2015Review
- Na+ channel function, regulation, structure, trafficking and sequestration.The Journal of physiology · 2015Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Late Na(+) current (I(NaL)) is a major component of the action potential plateau in human and canine myocardium. Since I(NaL) is increased in heart failure and ischemia, it represents a novel potential target for cardioprotection. However, the molecular identity of I(NaL) remains unclear. We tested the hypothesis that the cardiac Na(+) channel isoform (Na(v)1.5) is a major contributor to I(NaL) in adult dog ventricular cardiomyocytes (VCs). Cultured VCs were exposed to an antisense morpholino-based oligonucleotide (Na(v)1.5 asOligo) targeting the region around the start codon of Na(v)1.5 mRNA or a control nonsense oligonucleotide (nsOligo). Densities of both transient Na(+) current (I(NaT)) and I(NaL) (both in pA/pF) were monitored by whole cell patch clamp. In HEK293 cells expressing Na(v)1.5 or Na(v)1.2, Na(v)1.5 asOligo specifically silenced functional expression of Na(v)1.5 (up to 60% of the initial I(NaT)) but not Na(v)1.2. In both nsOligo-treated controls and untreated VCs, I(NaT) and I(NaL) remained unchanged for up to 5 days. However, both I(NaT) and I(NaL) decreased exponentially with similar time courses (tau = 46 and 56 h, respectively) after VCs were treated with Na(v)1.5 asOligo without changes in 1) decay kinetics, 2) steady-state activation and inactivation, and 3) the ratio of I(NaL) to I(NaT). Four days after exposure to Na(v)1.5 asOligo, I(NaT) and I(NaL) amounted to 68 +/- 6% (mean +/- SE; n = 20, P < 0.01) and 60 +/- 7% (n = 11, P < 0.018) of those in VCs treated by nsOligo, respectively. We conclude that in adult dog heart Na(v)1.5 sodium channels have a "functional half-life" of approximately 35 h (0.69tau) and make a major contribution to I(NaL).
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