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Simultaneous Electrophysiological Recording and Calcium Imaging of Suprachiasmatic Nucleus Neurons
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Las anomalías de señalización y fosforilación de proteínas relacionadas con el Ca2+ juegan un papel central en un
Yukiomi Tsuji1, Mayumi Hojo, Niels Voigt
1Department of Cardiovascular Research, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan. y-tsuji@hh.iij4u.or.jp
Circulation
|May 11, 2011
Resumen
La tormenta eléctrica (ES) en pacientes con desfibrilador cardioverter implantable implica cambios en las proteínas relacionadas con Ca2+. Este estudio revela que la activación de la proteína quinasa II dependiente de Ca2+/calmodulina y la desfosforilación de fosfolambano contribuyen a la promoción de la arritmia y la disfunción de la ES.
Área de la Ciencia:
- Cardiología Cardiología.
- Biología Molecular Biología Molecular
- Electrofisiología y electrofisiología.
Sus antecedentes:
- La tormenta eléctrica (ES) es una complicación grave en pacientes con cardioverter implantable y desfibrilador.
- Los mecanismos moleculares que subyacen a la ES siguen siendo poco conocidos.
- Este estudio introduce un nuevo modelo experimental para investigar la ES.
Objetivo del estudio:
- Investigar el papel de las alteraciones de las proteínas que manejan el calcio (Ca2+) en el desarrollo de la ES.
- Para dilucidar las bases moleculares del círculo vicioso en ES.
Principales métodos:
- Se utilizó un modelo de conejo con bloqueo atrioventricular completo y implantación implantable de cardioverter-desfibrilador.
- Se analizó la expresión y fosforilación de las proteínas manipuladoras de Ca2+ en los tejidos ventriculares.
- Se evaluaron los efectos de un antagonista de la calmodulina (W-7) en la ES y la función cardíaca.
Principales resultados:
- Los conejos de ES exhibieron un aumento de la hiperfosforilación de la proteína kinasa II (CaMKII) dependiente de la calmodulina y de la fosfolambana.
- La disfunción contráctil fue significativamente mayor en conejos ES en comparación con conejos no ES.
- El tratamiento con antagonistas de calmodulina redujo la hiperfosforilación CaMKII, suprimió las arritmias y mejoró la función cardíaca.
Conclusiones:
- La ES está asociada con una activación significativa de CaMKII y la desfosforilación de fosfolambano.
- Estos cambios moleculares contribuyen a la promoción de las arritmias y la disfunción mecánica en ES.
- La orientación de CaMKII puede ofrecer una estrategia terapéutica para el manejo de la ES.
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