Localisation of SCN10A gene product Na(v)1.8 and novel pain-related ion channels in human heart.

@article{Facer2011LocalisationOS,
  title={Localisation of SCN10A gene product Na(v)1.8 and novel pain-related ion channels in human heart.},
  author={P. Facer and P. Punjabi and A. Abrari and R. Kaba and N. Severs and J. Chambers and J. Kooner and P. Anand},
  journal={International heart journal},
  year={2011},
  volume={52 3},
  pages={
          146-52
        }
}
We have shown that the gene SCN10A encoding the sodium channel Na(v)1.8 is a susceptibility factor for heart block and serious ventricular arrhythmia. Since Na(v)1.8 is known to be present in nerve fibres that mediate pain, it may be related to both cardiac pain and dysrhythmia. The localisation of Na(v)1.8 and other key nociceptive ion channels, including Na(v)1.7, Na(v)1.9, capsaicin receptor TRPV1, and purinergic receptor P2X(3), have not been reported in human heart. The aim of this study… Expand
Novel SCN 3 B Mutation Associated With Brugada Syndrome Affects Intracellular Trafficking and Function of Nav 1 . 5
In cardiomyocytes, 5 distinct sodium channel β-subunits, Navβ1, Navβ1b, β2, β3 and β4, are known to be expressed. In particular, Navβ1 and Navβ3, encoded by SCN1B and SCN3B, are abundantly expressed,Expand
NaV1.8: a novel contributor to cardiac arrhythmogenesis in heart failure.
TLDR
The authors studied fresh left ventricular samples from 25 explanted hearts of patients with terminal HF and observed two times increase of NaV1.8 protein in HF samples when compared with non-failing donor hearts, caused by a comparable elevation of SCN10A mRNA, suggesting upregulation at the level of gene expression. Expand
Voltage-gated sodium channels in the mammalian heart
TLDR
When comparing the Na+ channel mRNA patterns in the heart of various mammalian species, only minute quantities of transcripts for TTX-sensitive Na+ channels were detectable in whole pig and human hearts, suggesting that these channels are not involved in cardiac excitation phenomena in higher mammals. Expand
[Progress in sodium channelopathies and biological functions of voltage-gated sodium channel blockers].
TLDR
A novel cysteine-rich secretory protein (CRBGP) has been isolated and purified from the buccal gland of the lampreys (Lampetra japonica), and it could inhibit the Na+ current of the hippocampus and dorsal root neurons for the first time. Expand
Blocking Scn10a Channels in Heart Reduces Late Sodium Current and Is Antiarrhythmic
TLDR
It is shown that low concentrations of A-803467 selectively block “late” sodium current and shorten action potentials in mouse and rabbit cardiomyocytes and represents a new target for antiarrhythmic intervention. Expand
Novel SCN3B mutation associated with brugada syndrome affects intracellular trafficking and function of Nav1.5.
TLDR
The Val110Ile mutation ofSCN3B is a relatively common cause of SCN5A-negative BrS in Japan, which has a reduced sodium current because of the loss of cell surface expression of Nav1.5. Expand
Exonic mutations in SCN9A (NaV1.7) are found in a minority of patients with erythromelalgia
TLDR
It is concluded that functionally characterized mutations of NaV1.7 (I848T) are present only in a minority of patient with EM, and the vast majority of those will most probably not be causally linked to their disease. Expand
Pathogenic mutations perturb calmodulin regulation of Nav1.8 channel.
TLDR
Findings indicate a role of CaM in the regulation of Nav1.8 channel function in cardiac arrhythmias, and show that CaM enhanced slow inactivation of the Nav1-8 channel and hyperpolarized steady-state inactivation curve of sodium currents. Expand
Tetrodotoxin-sensitive α-subunits of voltage-gated sodium channels are relevant for inhibition of cardiac sodium currents by local anesthetics
TLDR
The data demonstrate for the first time that cardiac TTX-sensitive sodium channels are relevant for inhibition of cardiac sodium currents by LAs. Expand
The G1662S NaV1.8 mutation in small fibre neuropathy: impaired inactivation underlying DRG neuron hyperexcitability
TLDR
It is reported for the first time a mutation of NaV1.8 which impairs inactivation, in patients with painful I-SFN, which indicates that an array of Nav1. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 53 REFERENCES
Exploring the role of nociceptor-specific sodium channels in pain transmission using Nav1.8 and Nav1.9 knockout mice
TLDR
Evidence is provided for a modulatory role of Na(v)1.9, and to a lesser extent Na(w)r1.8 in the development of cold, but not mechanical allodynia in neuropathic pain conditions, and results indicate that Na( v) 1.9 signaling might be involved in visceral pain. Expand
Modulation of the Cardiac Sodium Channel Nav1.5 by Fibroblast Growth Factor Homologous Factor 1B*
TLDR
It is shown that fibroblast growth factor homologous factor 1B binds to the C terminus of the cardiac voltage-gated sodium channel Nav1.5 and modulates the properties of the channel, the first report showing that interaction with a growth factor can modulate properties of a voltage- gated sodiumChannel. Expand
The voltage-gated sodium channel Nav1.9 is required for inflammation-based urinary bladder dysfunction
TLDR
It is concluded that the Nav1.9 sodium channel provides an important link between inflammatory processes and changes in urodynamic properties that occur during urinary bladder inflammation. Expand
Genetic variation in SCN10A influences cardiac conduction
TLDR
It is shown that SCN10A is expressed in mouse and human heart tissue and that PR interval is shorter in Scn10a−/− mice than in wild-type mice, and that rs6795970 is associated with a higher risk of heart block and a lower risk of ventricular fibrillation. Expand
Specific pattern of ionic channel gene expression associated with pacemaker activity in the mouse heart
TLDR
The present study provides the first genome‐scale regional ionic channel expression profile in the mouse heart by using large‐scale real‐time RT‐PCR and two‐way hierarchical clustering analysis of the 71 genes successfully classified the six pools from the four distinct regions. Expand
Sodium channel Nav1.8 immunoreactivity in painful human dental pulp
TLDR
Fibres immunoreactive for Nav1.8, the tetrodotoxin-resistant voltage-gated sodium channel expressed by nociceptors, were significantly increased on image analysis in the painful group, suggesting it may represent a therapeutic target in trigeminal nerve pain states. Expand
P2X2/3 receptor activity of rat nodose ganglion neurons contributing to myocardial ischemic nociceptive signaling
TLDR
The present results have shown that the sensitivity of P2X(2/3) receptor in nodose ganglion neurons was increased after myocardial ischemic injury under electrophysiological observation, which indicates that the activity of P1/3 receptors in NG neurons was involved in the transmission of myocardials nociceptive signal. Expand
Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger
TLDR
It is suggested that accumulation of SNS/PN3 and/or loss of GDNF may contribute to pain in causalgia, and that selective blockers of S NS/PN 3 and/ or rhGDNF may provide effective novel treatments. Expand
Expression of neuropeptide Y and its receptors Y1 and Y2 in the rat heart and its supplying autonomic and spinal sensory ganglia in experimentally induced diabetes
TLDR
Data show that a disturbance of the cardiac NPY-Y1R/Y2R signaling system develops slowly in the course of experimentally induced diabetes and differentially affects atria and ventricles in diabetic cardiac autonomic neuropathy. Expand
Localization of Nav1.5 sodium channel protein in the mouse brain
TLDR
Results suggest that Nav1.5 protein may play a role in the physiology of the central nervous system (generation and propagation of electrical signals by axons) through co-localized with neurofilaments and clustered in the neuronal processes, mainly axons. Expand
...
1
2
3
4
5
...