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Las hemooxigenasas de las células musculares lisas vasculares generan el monóxido de carbono estimulante de la
N Christodoulides1, W Durante, M H Kroll
1Houston (Tex) Veterans Affairs Medical Center 77030, USA.
Circulation
|May 1, 1995
Resumen
Las células del músculo liso vascular (CMS) producen monóxido de carbono (CO) a través de la actividad de la hemooxigenasa (HO). Este CO estimula la producción de GMPc en las SMC y las plaquetas, lo que indica una nueva vía de señalización.
Área de la Ciencia:
- Biología Vascular Biología Vascular
- La señalización celular.
- La bioquímica es la bioquímica.
Sus antecedentes:
- El monóxido de carbono (CO) y el óxido nítrico (NO) activan la guanylil ciclasa soluble, aumentando el cGMP intracelular.
- Las hemooxigenasas (HO) son enzimas que metabolizan el hemo.
Objetivo del estudio:
- Para investigar la producción endógena de CO por las células del músculo liso vascular (SMC).
- Determinar el papel de las hemooxigenasas (HO) en la generación de CO dentro de las SMC.
- Evaluar el impacto del CO derivado de SMC en los niveles de GMPc.
Principales métodos:
- Se utilizaron SMC aórticas de rata cultivadas (RASMC).
- Se evaluó la expresión de la hemooxigenasa-1 (HO-1) y la hemooxigenasa-2 (HO-2).
- Las RASMC fueron tratadas con inductores HO-1 (hemina, arsenita de sodio).
- Se midieron los niveles de cGMP en las RASMC y las plaquetas co-cubadas.
- Se utilizó un inhibidor de la oxigenasa hemo (protoporfirina de zinc IX).
Principales resultados:
- Las RASMC expresan tanto HO-1 como HO-2.
- La inducción de HO-1 aumentó el cGMP en las RASMC y las plaquetas.
- La producción de CO inducida por las RASMCs elevó la cGMP plaquetaria.
- La actividad de la NO sintasa no estuvo involucrada en los aumentos observados de GMPc.
- La inhibición de la hemooxigenasa revirtió las elevaciones de GMPc.
Conclusiones:
- Las SMCs vasculares poseen actividad constitutiva e inducible de la hemooxigenasa.
- Las SMCs generan CO que estimula la guanylil ciclasa en las SMCs y las plaquetas.
- Esto pone de relieve una nueva vía de señalización endógena mediada por CO en las células vasculares.
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