Key result
Acute disruption of the NKA/AnkB interaction using a disruptor peptide abolished the correlation between NKA and NCX currents and increased the rate of Ca2+ sparks and waves in cardiomyocytes.
Why the study?
It was unclear to what extent NKA binding to AnkB regulates local Na+ and Ca2+ domains and NCX activity in cardiomyocytes.
Does disruption of the NKA/AnkB interaction alter local Na+ and Ca2+ domains and NCX activity in cardiomyocytes?
Population
Adult rat ventricular myocytes and cardiomyocytes from AnkB+/- mice
Comparison
MAB peptide disruptor vs control and AnkB+/- mice
Design
Preclinical experimental study
Authors
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Highlights potential arrhythmogenic Ca2+ dysregulation in Ankyrin B syndrome; leaves open translation to human disease.
Does disruption of the NKA/AnkB interaction alter local Na+ and Ca2+ domains and NCX activity in cardiomyocytes?
Disruption of the AnkB/NKA/NCX domain increases the rate of Ca2+ sparks and waves via the NKAα2 isoform, suggesting a pathophysiological mechanism for arrhythmias in Ankyrin B syndrome.
Skogestad et al. (2019) studied AnkB syndrome. MAB peptide (disruptor peptide) vs. Control was evaluated on Correlation between NKA and NCX currents and frequency of Ca2+ sparks and waves. Acute disruption of the NKA/AnkB interaction using a disruptor peptide abolished the correlation between NKA and NCX currents and increased the rate of Ca2+ sparks and waves in cardiomyocytes.
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