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Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
Proteína de choque térmico citosólico 60, hipoxia y apoptosis
1Baylor College of Medicine and the VA Medical Center, Houston, Tex, USA.
Circulation
|November 20, 2002
Resumen
La hipoxia hace que la proteína de choque térmico 60 (HSP60) se desprenda de bax, liberando a bax para que se mueva a las mitocondrias y desencadene la apoptosis. Esta disociación es clave para la muerte celular durante la privación de oxígeno.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- La bioquímica es la bioquímica.
Sus antecedentes:
- La proteína de choque térmico 60 (HSP60) es principalmente mitocondrial, pero también se encuentra en el citosol.
- HSP60 normalmente tiene complejos con bax en el citosol, inhibiendo la translocación de bax a las mitocondrias y la apoptosis.
- Se planteó la hipótesis de que la hipoxia / reoxigenación reducía el HSP60, promoviendo la translocación de bax y la liberación del citocromo c.
Objetivo del estudio:
- Para investigar el papel de HSP60 en la apoptosis durante la hipoxia / reoxigenación.
- Para determinar si la reducción de HSP60 precipita la translocación de bax y la liberación del citocromo c.
- Para dilucidar el mecanismo de la interacción HSP60-bax bajo condiciones hipóxicas.
Principales métodos:
- Los miocitos cardíacos de ratas adultas fueron sometidos a hipoxia y reoxigenación.
- Se midieron los niveles de HSP60, HSP72, bax y bcl-2.
- El fraccionamiento celular y la co-inmunoprecipitación se utilizaron para analizar la localización e interacciones de las proteínas.
- Se evaluó la liberación del citocromo c.
Principales resultados:
- Los niveles de HSP60 disminuyeron durante la reoxigenación, mientras que los de HSP72 aumentaron.
- Los niveles de Bax y bcl-2 disminuyeron durante la reoxigenación.
- La liberación del citocromo c se produjo al final de la hipoxia, antes de la reoxigenación.
- La hipoxia causó la disociación del complejo HSP60-bax; el HSP60 citosólico se translocó a la membrana plasmática y el bax se translocó a las mitocondrias.
Conclusiones:
- La hipoxia induce la disociación del complejo HSP60-bax.
- La translocación del HSP60 citosólico a la membrana plasmática y el bax a las mitocondrias desencadena la apoptosis.
- Esta disociación del complejo HSP60-bax es suficiente para iniciar la muerte celular programada.
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