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La fosforilación del canal de sodio regulado por voltaje en Ser571 regula la corriente tardía, la arritmia y la

Patric Glynn¹, Hassan Musa¹, Xiangqiong Wu¹

¹From Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus (P.G., H.M., X.W., S.D.U., S.L., L.Q., P.J.W., P.B.R., S.G., P.J.M., T.J.H.); Department of Biomedical Engineering, College of Engineering, The Ohio State University, Columbus (P.G., X.W., S.D.U., L.Q., T.J.H.); Departments of Physiology & Cell Biology (H.M., S.L., P.J.W., P.B.R., S.G., P.J.M.) and Internal Medicine (P.J.M., T.J.H.), The Ohio State University Wexner Medical Center, Columbus; and Division of Pharmacy Practice and Administration, College of Pharmacy, The Ohio State University, Columbus (P.B.R.).

|July 19, 2015

Resumen

El estudio revela que el Ser571 en los canales Nav1.5 es crucial para la corriente tardía de sodio (INa,L) y promueve las arritmias. Este hallazgo ofrece información sobre la activación de INa,L dependiente de CaMKII y posibles objetivos terapéuticos.

Área de la Ciencia:

Fisiología cardiovascular
Cardiología molecular
Regulación del canal iónico

Sus antecedentes:

Los canales de sodio regulados por voltaje (Nav) son críticos para la actividad eléctrica cardíaca.
Una corriente de sodio tardía persistente (INa,L) contribuye a la enfermedad cardíaca.
La quinasa II dependiente de la calmodulina (CaMKII) activa el INa,L, pero su mecanismo in vivo no está claro.

Objetivo del estudio:

Investigar el papel in vivo del Ser571 en el canal Nav1.5.
Para aclarar el mecanismo molecular de la regulación INa,L dependiente de CaMKII.

Principales métodos:

Modelos de ratón Scn5a generados con mutaciones Ser571 fosfomiméticas (S571E) y abladas (S571A).
Se han realizado estudios electrofisiológicos para evaluar la función del canal.
Función cardíaca evaluada a nivel celular y animal y susceptibilidad a las arritmias.

Principales resultados:

Ser571 regula específicamente las propiedades de INa,L, no las de otras propiedades relacionadas con CaMKII.
El aumento de INa,L debido a Ser571 promueve la repolarización anormal y el manejo de Ca2+.
Ser571 es esencial para las arritmias inducidas por sobrecarga de presión y la remodelación desadaptativa.

Conclusiones:

Proporcionó la primera evidencia in vivo para la activación de CaMKII del INa,L patógeno a través de Ser571.
Se ha demostrado que la regulación dependiente de Ser571 de Nav1.5 modula específicamente el INa,L.
Los resultados apoyan el diseño racional de fármacos para terapias dirigidas a INa,L.

Palabras clave:

Corriente de Na+potencial de acción arritmias cardíacas Proteína quinasa dependiente de calcio y calmodulina tipo 2 canales iónicos

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