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Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
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El aumento de la fuga de Ca2+ del retículo sarcoplasmático y el aumento de la función del intercambiador de Na+-Ca2+
Niels Voigt1, Na Li, Qiongling Wang
1Division of Experimental Cardiology, Medical Faculty Mannheim, University of Heidelberg, Germany.
Circulation
|March 30, 2012
Resumen
En pacientes con fibrilación auricular, el aumento de la fuga de Ca2+ del retículo sarcoplásmico, impulsado por la proteína quinasa II (CaMKII) y los receptores de ryanodina (RyR2), promueve ritmos cardíacos peligrosos.
Área de la Ciencia:
- Cardiología Cardiología.
- Biología Molecular Biología Molecular
- Electrofisiología y electrofisiología.
Sus antecedentes:
- Las despolarizaciones posteriores tardías (DADs) mediadas por la corriente de intercambio Na(+) -Ca(2+) (I(NCX)) pueden desencadenar fibrilación auricular (AF).
- Los mecanismos subyacentes a las DAD en pacientes con AF siguen sin estar claros.
Objetivo del estudio:
- Para investigar los mecanismos de las DAD en pacientes con FA crónica (FAc).
- Para identificar las alteraciones moleculares en el retículo sarcoplásmico (SR) Ca2+) y la función RyR2 en cAF.
Principales métodos:
- Análisis de muestras auriculares derechas de pacientes de control y pacientes con FAC usando Western blot, pinza de parche y imágenes de Fluo-3.
- Medición de la fuga de SR Ca2+, la probabilidad de apertura de RyR2 y la fosforilación de proteínas.
- Inhibición farmacológica de CaMKII y de la proteína quinasa A.
- Estudios en ratones knock-in con una fosforilación RyR2 alterada.
Principales resultados:
- Los pacientes con AFc exhibieron fugas significativamente más altas de Ca2+ y una mayor probabilidad de apertura de RyR2.
- Se observó un aumento de la expresión y la actividad de CaMKII y la fosforilación de RyR2 en sitios específicos en cAF.
- La inhibición de CaMKII redujo la fuga de Ca2+ de la SR y los eventos de liberación espontánea de Ca2+.
- I ((NCX) se regulaba en cAF, y la ganancia de acoplamiento diastólico [Ca ((2+) ] ((i) de tensión se elevó.
Conclusiones:
- La filtración mejorada de SR Ca ((2+) a través de RyR2 hiperfosforilado por CaMKII es un mecanismo clave para los DAD en la FAc.
- El aumento de I ((NCX) y el aumento de la ganancia de acoplamiento de tensión diastólica [Ca (((2+) ] ((i) contribuyen a la promoción de la AF.
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