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Isolation, Culture, and Functional Characterization of Adult Mouse Cardiomyoctyes

Isolation, Culture, and Functional Characterization of Adult Mouse Cardiomyoctyes

Published on: September 25, 2013

MEF2 activa un programa genético que promueve la dilatación de la cámara y la disfunción contráctil en la

Ralph J van Oort¹, Eva van Rooij, Meriem Bourajjaj

¹Hubrecht Laboratory, and Interuniversity Cardiology Institute Netherlands, Royal Netherlands Academy of Sciences, Utrecht, Netherlands.

|July 19, 2006

Resumen

Los factores de transcripción del factor potenciador de miocitos-2 (MEF2) promueven la dilatación y la disfunción de la cámara cardíaca, no el crecimiento, en el corazón postnatal. La inhibición de MEF2 normalizó las dimensiones y la función cardíaca en ratones con cardiomiopatía hipertrófica.

Área de la Ciencia:

Biología Cardiovascular Biología Cardiovascular
Cardiología Molecular Cardiología Molecular
Regulación genética Reglamento genético.

Sus antecedentes:

La hipertrofia cardíaca es un factor de riesgo para la mortalidad por enfermedad cardíaca.
El factor 2 potenciador de miocitos (MEF2) es un factor de transcripción clave en las vías hipertróficas cardíacas.
El papel preciso de MEF2 en la remodelación cardíaca no se entiende completamente.

Objetivo del estudio:

Para aclarar la función de los factores de transcripción MEF2 en la remodelación cardíaca postnatal.
Para investigar la interacción entre MEF2 y la señalización de la calcineurina en el corazón.
Evaluar el impacto de la inhibición del MEF2 en la función cardíaca y la expresión génica.

Principales métodos:

Utilizó la transgénesis condicional para expresar un MEF2 negativo dominante en corazones murinos.
Empleó imágenes de resonancia magnética para evaluar la remodelación cardíaca en la hipertrofia inducida por calcineurina.
Se realizó un perfil de microarrays para identificar genes regulados por MEF2.

Principales resultados:

La inhibición del MEF2 normalizó las dimensiones ventriculares y la contractilidad en corazones hipertrofiados.
La sobreexpresión de MEF2A condujo a la dilatación de la cámara cardíaca.
El MEF2 regula los genes involucrados en los procesos nucleares, el citoesqueleto y las mitocondrias.

Conclusiones:

Los factores de transcripción MEF2 tienen un papel novedoso en el corazón postnatal.
La activación de MEF2 tiene un impacto mínimo en el crecimiento cardíaco, pero promueve la dilatación de la cámara y la disfunción mecánica.
MEF2 contribuye al desarrollo de la cardiomiopatía dilatada.

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