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Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel
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El inhibidor del activador del plasminógeno-1 y su cofactor vitronectina estabilizan la trombosis arterial después de
S Konstantinides1, K Schäfer, T Thinnes
1Department of Vascular Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.
Circulation
|February 7, 2001
Resumen
El inhibidor del activador del plasminógeno-1 (PAI-1) y la vitronectina (VN) previenen la ruptura prematura del coágulo y la embolización en la trombosis arterial. PAI-1 se sintetiza localmente, mientras que VN se origina en el plasma.
Área de la Ciencia:
- Biología Cardiovascular Biología Cardiovascular
- La hemostasis y la trombosis.
- La medicina molecular es una medicina molecular.
Sus antecedentes:
- Se debaten las funciones del inhibidor-1 del activador del plasminógeno (PAI-1) y la vitronectina (VN) en la trombosis y la trombolisis arterial.
- Comprender sus contribuciones in vivo es crucial para el desarrollo de terapias dirigidas.
Objetivo del estudio:
- Investigar las contribuciones específicas de PAI-1 y VN a la formación y estabilidad de trombos arteriales.
- Para aclarar los orígenes de la acumulación de PAI-1 y VN en los sitios de lesión vascular.
Principales métodos:
- Inducción de la lesión de la arteria carótida utilizando cloruro férrico en ratones tipo salvaje, PAI-1 knockout y VN knockout.
- Evaluación de la oclusión trombótica, el tiempo hasta la oclusión, la estabilidad del trombo y las tasas de permeabilidad.
- Análisis histoquímicos y de expresión génica (RT-PCR) para determinar la localización y síntesis de PAI-1 y VN.
Principales resultados:
- Los ratones con deficiencia de PAI-1 exhibieron una oclusión trombótica reducida y retrasada en comparación con el tipo salvaje.
- Los ratones con deficiencia de VN mostraron trombos inestables propensos a la embolización, lo que condujo a tasas de patencia más altas.
- La expresión de PAI-1 fue regulada localmente en los trombos y las paredes de los vasos sanguíneos, mientras que la proteína VN se acumuló en el plasma.
Conclusiones:
- PAI-1 y VN son críticos para prevenir la disolución prematura del trombo y la embolización después de una lesión arterial.
- PAI-1 contribuye a la estabilidad del trombo a través de la síntesis local.
- El papel de VN en la estabilización del trombo parece estar mediado por proteínas derivadas del plasma.
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