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El óxido nítrico regula la exocitosis mediante la S-nitrosilación del factor sensible al N-etilmaleimida
Kenji Matsushita1, Craig N Morrell, Beatrice Cambien
1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Cell
|October 22, 2003
Resumen
El óxido nítrico (NO) previene la inflamación vascular al inhibir la liberación de moléculas inflamatorias de las células endoteliales. Esto se logra al NO regular la actividad del factor sensible a la N-etilmaleimida (NSF), una proteína clave en el transporte celular.
Área de la Ciencia:
- La bioquímica es la bioquímica.
- Biología celular Biología celular.
- Inmunología Inmunología.
Sus antecedentes:
- Se sabe que el óxido nítrico (NO) posee propiedades antiinflamatorias en la vasculatura.
- Los mecanismos moleculares precisos que subyacen a los efectos antiinflamatorios del NO, particularmente en lo que respecta a la función de las células endoteliales, siguen sin ser esclarecidos en gran medida.
Objetivo del estudio:
- Investigar la base molecular por la cual el óxido nítrico (NO) ejerce sus efectos antiinflamatorios en la vasculatura.
- Identificar los procesos celulares específicos regulados por el NO que contribuyen a su acción antiinflamatoria.
Principales métodos:
- Investigó el efecto del NO en la exocitosis de los cuerpos de Weibel-Palade (WPB) en las células endoteliales.
- Se utilizaron ensayos bioquímicos para examinar la regulación de la actividad del factor sensible a la N-etilmaleimida (FNS) por NO.
- Analizó la nitrosilación de los residuos de cisteína en la NSF y su impacto en el desmontaje del complejo del receptor de proteínas de unión solubles de la NSF (SNARE).
Principales resultados:
- Se demostró que el óxido nítrico (NO) inhibe la exocitosis de los cuerpos de Weibel-Palade (WPB).
- NO regula la actividad del factor sensible a la N-etilmaleimida (NSF), una proteína clave en la exocitosis.
- NO inhibe el desmontaje mediado por NSF de los complejos SNARE a través de la nitrosilación de los residuos críticos de cisteína en NSF.
Conclusiones:
- El óxido nítrico (NO) inhibe la inflamación vascular al suprimir la exocitosis WPB a través de la regulación de la actividad NSF.
- El efecto inhibidor del NO en la NSF implica la nitrociliación de los residuos críticos de cisteína, lo que perjudica la función del complejo SNARE.
- Este mecanismo pone de relieve un papel novedoso para el NO en la regulación de la exocitosis a través de varios procesos fisiológicos, incluyendo la inflamación, la neurotransmisión y las respuestas inmunes.
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