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G alpha (i) y G alpha (o) son proteínas objetivo de las especies reactivas de oxígeno
M Nishida1, Y Maruyama, R Tanaka
1Laboratory of Pharmacology and Toxicology, Graduate School of Pharmaceutical Science, University of Tokyo, Japan.
Nature
|December 2, 2000
Resumen
Las especies reactivas de oxígeno (ROS) activan la quinasa regulada por señal extracelular (ERK) en las células cardíacas. El peróxido de hidrógeno se dirige directamente a las proteínas G alpha (i) y G alpha (o), iniciando esta vía de señalización crítica.
Área de la Ciencia:
- Biología Cardiovascular Biología Cardiovascular
- La señalización celular de las células.
- El estrés oxidativo Investigación de la investigación
Sus antecedentes:
- Las especies reactivas de oxígeno (ROS) median eventos clave de señalización, incluida la lesión cardíaca y la hipertrofia.
- La quinasa regulada por la señal extracelular (ERK) es una quinasa sensible a ROS conocida, pero su objetivo inicial de ROS sigue sin identificarse.
- Investigaciones anteriores implicaron a las tirosinacinasas y las pequeñas proteínas G en la activación de ERK inducida por ROS.
Objetivo del estudio:
- Para identificar la proteína diana inicial de ROS responsable de la activación de ERK en los cardiomiocitos.
- Para aclarar el papel de las subunidades de proteína G en la señalización ERK mediada por ROS.
Principales métodos:
- Se utilizaron cardiomiocitos neonatales de rata para estudiar la activación de ERK inducida por peróxido de hidrógeno (H2O2).
- Investigó la participación de las subunidades betagamma de la proteína G (G betagamma), la fosfatidilinositol-3-cinasa y el Src.
- Se realizaron estudios in vitro utilizando proteínas Gi y Go heterotriméricas purificadas y ensayos de unión [35S]GTP-gammaS.
Principales resultados:
- La inhibición de la activación de ERK inducida por G betagamma atenuada por H2O2.
- La activación de ERK inducida por H2O2 requería fosfatidilinositol-3-cinasa y Src, independientes de los ligandos del receptor acoplado a Gi.
- H2O2 activó directamente las proteínas purificadas Gi y Go, con modificaciones observadas en la subunidad G alfa, lo que condujo a la disociación.
Conclusiones:
- Las proteínas G alpha (i) y G alpha (o) son objetivos críticos del estrés oxidativo en la vía que conduce a la activación de la ERK.
- Este estudio revela un nuevo mecanismo de señalización de ROS en el corazón que implica la activación directa de la proteína G.
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