Conditional knockout of Fgf13 in murine hearts increases arrhythmia susceptibility and reveals novel ion channel modulatory roles.

ABSTRACT: The intracellular fibroblast growth factors (iFGF/FHFs) bind directly to cardiac voltage gated Na⁺ channels, and modulate their function. Mutations that affect iFGF/FHF-Na⁺ channel interaction are associated with arrhythmia syndromes. Although suspected to modulate other ionic currents, such as Ca²⁺ channels based on acute knockdown experiments in isolated cardiomyocytes, the in vivo consequences of iFGF/FHF gene ablation on cardiac electrical activity are still unknown. We generated inducible, cardiomyocyte-restricted Fgf13 knockout mice to determine the resultant effects of Fgf13 gene ablation. Patch clamp recordings from ventricular myocytes isolated from Fgf13 knockout mice showed a ~25% reduction in peak Na⁺ channel current density and a hyp

SUBMITTER: Wang X 

PROVIDER: S-EPMC5637556 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature