Key result
Knockdown of KCNE2 prolonged action potential duration and decreased transient outward K(+) current densities in neonatal and adult myocytes, whereas overexpression shortened APD in neonatal cells.
Why the study?
Does bidirectional modulation of KCNE2 expression affect action potential duration and voltage-dependent K+ channels in rat and mouse ventricular myocytes?
Population
Cultured neonatal and adult rat or neonatal mouse ventricular myocytes
Comparison
Bidirectional modulation of KCNE2 expression… vs Control myocytes (implied)
Design
Preclinical
Authors
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KCNE2 perturbation may predispose to ventricular arrhythmia; hypothesis-generating for human electrophysiology studies.
Does bidirectional modulation of KCNE2 expression affect action potential duration and voltage-dependent K+ channels in rat and mouse ventricular myocytes?
Endogenous KCNE2 is important in maintaining cardiac electrical stability by regulating Ito and APD, and its perturbation may predispose the heart to ventricular arrhythmia.
Liu et al. (2015) studied this question. Bidirectional modulation of KCNE2 expression vs. Baseline/unmodified cells was evaluated on Action potential duration and voltage-dependent K(+) channels. Knockdown of KCNE2 prolonged action potential duration and decreased transient outward K(+) current densities in neonatal and adult myocytes, whereas overexpression shortened APD in neonatal cells.
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