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Inducción del inhibidor del activador del plasminógeno por productos liberados de las plaquetas
1Cardiovascular Division, Washington University School of Medicine, St. Louis, Missouri 63110.
Circulation
|October 1, 1990
Resumen
La activación de las plaquetas libera factores de crecimiento que aumentan el inhibidor del activador del plasminógeno-I (IAP) en la sangre. Este hallazgo sugiere que las plaquetas contribuyen a los niveles elevados de IAP observados durante el infarto de miocardio.
Área de la Ciencia:
- Biología Cardiovascular Biología Cardiovascular
- La hemostasis y la trombosis.
- La medicina molecular es una medicina molecular.
Sus antecedentes:
- La activación plaquetaria y el aumento de la actividad del inhibidor del activador del plasminógeno (IAP) tipo I están relacionados con el infarto agudo de miocardio.
- La relación entre la activación plaquetaria y la actividad de IAP tipo I requiere una investigación más profunda.
Objetivo del estudio:
- Para investigar la relación in vivo entre la activación plaquetaria y la actividad plasmática de IAP tipo I.
- Determinar el papel de los factores de crecimiento derivados de las plaquetas en la modulación de los niveles de IAP tipo I.
Principales métodos:
- Infusión de factor de crecimiento epidérmico, factor de crecimiento transformador beta y lisados plaquetarios en conejos.
- Medición de la actividad plasmática de la IAP y la expresión de ARN mensajero tipo 1 de la IAP.
- Administración de anticuerpos neutralizantes del factor de crecimiento anti-transformador beta.
Principales resultados:
- El factor de crecimiento epidérmico, el factor de crecimiento transformador beta y los lisatos plaquetarios aumentaron significativamente la actividad plasmática de IAP de manera dependiente de la dosis.
- Los lisatos de plaquetas se elevan notablemente en el ARN mensajero tipo 1 de la IAP plasmática en la aorta, el hígado y el miocardio.
- El anticuerpo beta del factor de crecimiento anti-transformador atenuó el aumento de la IAP plasmática, lo que indica el papel del TGF-beta.
Conclusiones:
- Los factores de crecimiento asociados a las plaquetas y los lisatos plaquetarios aumentan la IAP plasmática de tipo I in vivo.
- La activación de las plaquetas y la liberación de los factores de crecimiento asociados contribuyen a elevar los niveles plasmáticos de IAP después del infarto de miocardio.
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