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• W2036700841 abstract "Background— Timothy syndrome (TS) is a disease of excessive cellular Ca 2+ entry and life-threatening arrhythmias caused by a mutation in the primary cardiac L-type Ca 2+ channel (Ca V 1.2). The TS mutation causes loss of normal voltage-dependent inactivation of Ca V 1.2 current (I Ca ). During cellular Ca 2+ overload, the calmodulin-dependent protein kinase II (CaMKII) causes arrhythmias. We hypothesized that CaMKII is a part of the proarrhythmic mechanism in TS. Methods and Results— We developed an adult rat ventricular myocyte model of TS (G406R) by lentivirus-mediated transfer of wild-type and TS Ca V 1.2. The exogenous Ca V 1.2 contained a mutation (T1066Y) conferring dihydropyridine resistance, so we could silence endogenous Ca V 1.2 with nifedipine and maintain peak I Ca at control levels in infected cells. TS Ca V 1.2–infected ventricular myocytes exhibited the signature voltage-dependent inactivation loss under Ca 2+ buffering conditions, not permissive for CaMKII activation. In physiological Ca 2+ solutions, TS Ca V 1.2–expressing ventricular myocytes exhibited increased CaMKII activity and a proarrhythmic phenotype that included action potential prolongation, increased I Ca facilitation, and afterdepolarizations. Intracellular dialysis of a CaMKII inhibitory peptide, but not a control peptide, reversed increases in I Ca facilitation, normalized the action potential, and prevented afterdepolarizations. We developed a revised mathematical model that accounts for CaMKII-dependent and CaMKII-independent effects of the TS mutation. Conclusion— In TS, the loss of voltage-dependent inactivation is an upstream initiating event for arrhythmia phenotypes that are ultimately dependent on CaMKII activation." @default.
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• W2036700841 date "2008-11-25" @default.
• W2036700841 modified "2023-10-16" @default.
• W2036700841 title "Proarrhythmic Defects in Timothy Syndrome Require Calmodulin Kinase II" @default.
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• W2036700841 doi "https://doi.org/10.1161/circulationaha.108.788067" @default.
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