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Los polifosfatos de las plaquetas son mediadores proinflamatorios y procoagulantes in vivo
Felicitas Müller1, Nicola J Mutch, Wolfdieter A Schenk
1Department of Molecular Medicine and Surgery and Center for Molecular Medicine, Karolinska Institutet, Stockholm S-171 76, Sweden.
Cell
|December 17, 2009
Resumen
Las plaquetas activadas liberan polifosfato inorgánico (polyP), una molécula que desencadena la inflamación y la coagulación de la sangre. La orientación del poliP con fosfatasas redujo la trombosis y la inflamación impulsadas por plaquetas en ratones.
Área de la Ciencia:
- La bioquímica es la bioquímica.
- Hematología Hematología.
- Inmunología Inmunología.
Sus antecedentes:
- Las plaquetas son cruciales en la hemostasis, la trombosis y la inflamación.
- Los mecanismos moleculares que vinculan las plaquetas a estos procesos están siendo investigados.
Objetivo del estudio:
- Para investigar el papel del polifosfato inorgánico (polyP) liberado por las plaquetas activadas.
- Para determinar la participación de la poliP en la trombosis, la inflamación y la coagulación.
Principales métodos:
- Investigó la unión de poliP al factor XII y su activación.
- Se evaluó el efecto de la poliP en la liberación de bradicinina y la permeabilidad vascular en ratones.
- Estudió el impacto del factor XII, los receptores de bradicinina y las fosfatasas en los efectos mediados por poliP.
- Se examinó el papel de la poliP en los modelos de coagulación plasmática y embolia pulmonar.
- Se analizó el efecto de la poliP en el plasma de pacientes con síndrome de Hermansky-Pudlak.
Principales resultados:
- Las plaquetas activadas liberan poliP, que activa el factor XII y desencadena la liberación de bradicinina.
- PolyP aumenta la permeabilidad vascular y la extravasación de fluidos, efectos dependientes del factor XII y los receptores de bradicinina.
- PolyP inicia la coagulación plasmática a través de la vía de contacto y causa una embolia pulmonar letal.
- La focalización del poliP con fosfatasas inhibe la actividad procoagulante plaquetaria y la trombosis.
- La adición de PolyP corrige la coagulación defectuosa en el plasma de pacientes con síndrome de Hermansky-Pudlak.
Conclusiones:
- El polifosfato inorgánico (polyP) es un nuevo mediador liberado por las plaquetas activadas.
- PolyP juega un papel fundamental en los trastornos inflamatorios y procoagulantes impulsados por las plaquetas.
- La orientación hacia el poliP presenta una estrategia terapéutica potencial para las afecciones trombóticas e inflamatorias.
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