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El producto del gen bcl-2 previene la muerte celular programada de los miocitos ventriculares
L A Kirshenbaum1, D de Moissac
1Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre, Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada. Lorrie@SBRC.umanitoba.ca
Circulation
|October 7, 1997
Resumen
La proteína antiapoptótica bcl-2 previene la muerte celular programada en las células del músculo cardíaco provocada por p53. Este estudio demuestra que el bcl-2
Área de la Ciencia:
- Biología Cardiovascular Biología Cardiovascular
- Biología Molecular Biología Molecular
- Investigación de la Muerte Celular.
Sus antecedentes:
- La muerte celular programada (apoptosis) es crucial en el músculo cardíaco.
- p53 es un inductor conocido de la apoptosis en varios tipos de células.
- El papel de bcl-2 en la prevención de la apoptosis de los miocitos cardíacos requiere investigación.
Objetivo del estudio:
- Para determinar si la proteína antiapoptótica bcl-2 puede prevenir la apoptosis inducida por p53 en las células del músculo cardíaco (miocitos ventriculares).
Principales métodos:
- Utilizó el adenovirus de replicación defectuosa para entregar genes bcl-2 y p53 a los miocitos ventriculares.
- Se evaluó la muerte celular de los miocitos utilizando la tinción vital.
- La apoptosis evaluada a través de la fragmentación del ADN y el etiquetado final de la transferasa terminal de desoxinucleótido.
- Se midieron los niveles de transcripción del promotor de bax.
Principales resultados:
- p53 aumentó significativamente la muerte de los miocitos ventriculares y la apoptosis.
- p53 también aumentó la transcripción del promotor de bax.
- La expresión de bcl-2 impidió la muerte y la apoptosis de los miocitos inducidas por p53.
- bcl-2 reprimió la transcripción bax dependiente de p53.
Conclusiones:
- bcl-2 funciona como un factor antiapoptótico en los miocitos ventriculares.
- Esta es la primera evidencia de la función antiapoptótica de bcl-2 en las células del músculo cardíaco.
- El efecto protector de bcl-2 está relacionado con la represión de la transcripción bax mediada por p53.
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