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El efecto antiinfarto de la activación del receptor de A2A-adenosina se debe principalmente a su acción sobre los
Zequan Yang1, Yuan-Ji Day, Marie-Claire Toufektsian
1Department of Biomedical Engineering, of Virginia Health System, Charlottesville 22903, USA. zy6b@virginia.edu
Circulation
|April 27, 2005
Resumen
La activación del receptor de adenosina A2A (A2AAR) con ATL146e reduce el tamaño del ataque cardíaco al atacar células derivadas de la médula ósea como los linfocitos. Este hallazgo aclara el mecanismo detrás de A2AARAR.
Área de la Ciencia:
- Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular
- Inmunología Inmunología.
- Farmacología Farmacología.
Sus antecedentes:
- La activación del receptor A2A de adenosina (A2AAR) después de la isquemia puede limitar el tamaño del infarto de miocardio.
- Los mecanismos celulares precisos que subyacen a los efectos cardioprotectores de A2AAR aún no se comprenden por completo.
Objetivo del estudio:
- Para aclarar los objetivos celulares de la activación de A2AAR responsable de reducir el tamaño del infarto.
- Investigar el papel de las células derivadas de la médula ósea en los efectos terapéuticos de los agonistas A2AAR.
Principales métodos:
- Se utilizaron modelos de ratones quiméricos (trasplante de médula ósea) para rastrear los orígenes celulares.
- Se administró un agonista selectivo de A2AAR (ATL146e) durante la reperfusión después de la isquemia miocárdica inducida.
- Se cuantificó el tamaño del infarto y los marcadores inflamatorios (mieloperoxidasa).
Principales resultados:
- ATL146e redujo significativamente el tamaño del infarto y la actividad de la mieloperoxidasa en ratones de tipo salvaje.
- Estos efectos protectores fueron abolidos en ratones A2AAR-knockout y cuando se utilizó un antagonista selectivo.
- Se identificaron las células derivadas de la médula ósea, específicamente los linfocitos, como los mediadores clave de los efectos de ahorro de infarto de ATL146e.
Conclusiones:
- La activación de A2AAR en las células derivadas de la médula ósea, en particular en los linfocitos T y B, media las acciones antiinfarto y antiinflamatorias de ATL146e.
- Estos hallazgos ponen de relieve un mecanismo crucial basado en células inmunes para la cardioprotección mediada por A2AAR durante la lesión por reperfusión.
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