scholarly journals Remodeling of Ion Channel Trafficking and Cardiac Arrhythmias

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2417
Author(s):  
Camille E. Blandin ◽  
Basile J. Gravez ◽  
Stéphane N. Hatem ◽  
Elise Balse
Keyword(s):  
Plasma Membrane ◽  
Ion Channels ◽  
Ion Channel ◽  
Cardiac Arrhythmias ◽  
Common Factors ◽  
Functional Expression ◽  
Cellular Level ◽  
Channel Trafficking ◽  
Genes Encoding ◽  
Ion Channel Trafficking

Both inherited and acquired cardiac arrhythmias are often associated with the abnormal functional expression of ion channels at the cellular level. The complex machinery that continuously traffics, anchors, organizes, and recycles ion channels at the plasma membrane of a cardiomyocyte appears to be a major source of channel dysfunction during cardiac arrhythmias. This has been well established with the discovery of mutations in the genes encoding several ion channels and ion channel partners during inherited cardiac arrhythmias. Fibrosis, altered myocyte contacts, and post-transcriptional protein changes are common factors that disorganize normal channel trafficking during acquired cardiac arrhythmias. Channel availability, described notably for hERG and KV1.5 channels, could be another potent arrhythmogenic mechanism. From this molecular knowledge on cardiac arrhythmias will emerge novel antiarrhythmic strategies.

scholarly journals Editorial: Ion Channel Trafficking and Cardiac Arrhythmias

2018 ◽  
Vol 9 ◽  
Author(s):  
Marcel A. G. van der Heyden ◽  
Brian P. Delisle ◽  
Hugues Abriel
Keyword(s):  
Ion Channel ◽  
Cardiac Arrhythmias ◽  
Channel Trafficking ◽  
Ion Channel Trafficking

scholarly journals Defining new insight into atypical arrhythmia: a computational model of ankyrin-B syndrome

2010 ◽  
Vol 299 (5) ◽  
pp. H1505-H1514 ◽  
Author(s):  
Roseanne M. Wolf ◽  
Colleen C. Mitchell ◽  
Matthew D. Christensen ◽  
Peter J. Mohler ◽  
Thomas J. Hund
Keyword(s):  
Ion Channels ◽  
Sarcoplasmic Reticulum ◽  
Ion Channel ◽  
Cardiac Arrhythmia ◽  
Cardiac Arrhythmias ◽  
Molecular Mechanisms ◽  
Sinus Node ◽  
Cellular Level ◽  
Cytoskeletal Proteins ◽  
Ankyrin B

Normal cardiac excitability depends on the coordinated activity of specific ion channels and transporters within specialized domains at the plasma membrane and sarcoplasmic reticulum. Ion channel dysfunction due to congenital or acquired defects has been linked to human cardiac arrhythmia. More recently, defects in ion channel-associated proteins have been associated with arrhythmia. Ankyrin-B is a multifunctional adapter protein responsible for targeting select ion channels, transporters, cytoskeletal proteins, and signaling molecules in excitable cells, including neurons, pancreatic β-cells, and cardiomyocytes. Ankyrin-B dysfunction has been linked to cardiac arrhythmia in human patients and ankyrin-B heterozygous (ankyrin-B+/−) mice with a phenotype characterized by sinus node dysfunction, susceptibility to ventricular arrhythmias, and sudden death (“ankyrin-B syndrome”). At the cellular level, ankyrin-B+/− cells have defects in the expression and membrane localization of the Na+/Ca2+ exchanger and Na+-K+-ATPase, Ca2+ overload, and frequent afterdepolarizations, which likely serve as triggers for lethal cardiac arrhythmias. Despite knowledge gathered from mouse models and human patients, the molecular mechanism responsible for cardiac arrhythmias in the setting of ankyrin-B dysfunction remains unclear. Here, we use mathematical modeling to provide new insights into the cellular pathways responsible for Ca2+ overload and afterdepolarizations in ankyrin-B+/− cells. We show that the Na+/Ca2+ exchanger and Na+-K+-ATPase play related, yet distinct, roles in intracellular Ca2+ accumulation, sarcoplasmic reticulum Ca2+ overload, and afterdepolarization generation in ankyrin-B+/− cells. These findings provide important insights into the molecular mechanisms underlying a human disease and are relevant for acquired human arrhythmia, where ankyrin-B dysfunction has recently been identified.

scholarly journals Non-conventional Axonal Organelles Control TRPM8 Ion Channel Trafficking and Peripheral Cold Sensing

Cell Reports ◽  
2020 ◽  
Vol 30 (13) ◽  
pp. 4505-4517.e5 ◽  
Author(s):  
Víctor Hugo Cornejo ◽  
Carolina González ◽  
Matías Campos ◽  
Leslie Vargas-Saturno ◽  
María de los Ángeles Juricic ◽  
...  
Keyword(s):  
Ion Channel ◽  
Channel Trafficking ◽  
Ion Channel Trafficking ◽  
Cold Sensing

scholarly journals Plasma membrane ion channels and epithelial to mesenchymal transition in cancer cells

2016 ◽  
Vol 23 (11) ◽  
pp. R517-R525 ◽  
Author(s):  
Iman Azimi ◽  
Gregory R Monteith
Keyword(s):  
Plasma Membrane ◽  
Ion Channels ◽  
Ion Channel ◽  
Cancer Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Therapeutic Resistance ◽  
Therapeutic Approaches ◽  
Mesenchymal Transition ◽  
Pharmacological Modulation ◽  
Channel Expression

A variety of studies have suggested that epithelial to mesenchymal transition (EMT) may be important in the progression of cancer in patients through metastasis and/or therapeutic resistance. A number of pathways have been investigated in EMT in cancer cells. Recently, changes in plasma membrane ion channel expression as a consequence of EMT have been reported. Other studies have identified specific ion channels able to regulate aspects of EMT induction. The utility of plasma membrane ion channels as targets for pharmacological modulation make them attractive for therapeutic approaches to target EMT. In this review, we provide an overview of some of the key plasma membrane ion channel types and highlight some of the studies that are beginning to define changes in plasma membrane ion channels as a consequence of EMT and also their possible roles in EMT induction.

scholarly journals Physical and functional interaction of KV 10.1 with Rabaptin-5 impacts ion channel trafficking

FEBS Letters ◽  
2012 ◽  
Vol 586 (19) ◽  
pp. 3077-3084 ◽  
Author(s):  
Milena Ninkovic ◽  
Mišo Mitkovski ◽  
Tobias Kohl ◽  
Walter Stühmer ◽  
Luis A. Pardo
Keyword(s):  
Ion Channel ◽  
Functional Interaction ◽  
Channel Trafficking ◽  
Ion Channel Trafficking
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