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Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
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Regulación genética de la estructura y función de la fibrina: las complejas interacciones entre genes y medio
Bernard C B Lim1, Robert A S Ariëns, Angela M Carter
1Academic Unit of Molecular Vascular Medicine, University of Leeds, Leeds, UK.
Lancet (London, England)
|May 3, 2003
Resumen
Las variaciones genéticas en el fibrinógeno y el factor XIII influyen en la estructura del coágulo de fibrina. Estas interacciones, junto con los niveles de fibrinógeno, tienen un impacto en el riesgo aterotrombótico, resolviendo las discrepancias de estudios anteriores.
Área de la Ciencia:
- La bioquímica es la bioquímica.
- Genética La genética.
- Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular
Sus antecedentes:
- Los polimorfismos en los genes del fibrinógeno y del factor XIII están relacionados con el riesgo aterotrombótico.
- Los estudios clínicos y de laboratorio muestran hallazgos inconsistentes con respecto a estas asociaciones.
- Las investigaciones anteriores no han aclarado completamente los mecanismos detrás de estas observaciones.
Objetivo del estudio:
- Para investigar las interacciones entre el factor XIII y los polimorfismos del gen del fibrinógeno.
- Examinar la relación entre las concentraciones de fibrinógeno y la estructura/función de la fibrina.
- Para aclarar el impacto de estos factores en el riesgo cardiovascular.
Principales métodos:
- Se emplearon análisis de permeación y microscopía electrónica.
- Se estudiaron las interacciones entre la estructura de la fibrina, el factor XIII Val34Leu y los polimorfismos del fibrinógeno (Aalpha Thr312Ala, Bbeta Arg448Lys).
- Se realizaron análisis tanto en plasma como en sistemas purificados.
Principales resultados:
- Las concentraciones más altas de fibrinógeno se correlacionan con una menor permeabilidad de la fibrina.
- Los alelos del factor XIII 34Val dieron lugar a coágulos de fibrina más apretados en comparación con los alelos 34Leu.
- El fibrinógeno Aalpha 312Ala también afectó la permeabilidad de la fibrina, similar a 312Thr.
Conclusiones:
- Los polimorfismos codificantes en el fibrinógeno y el factor XIII interactúan con las concentraciones de fibrinógeno para modificar la estructura y la función de la fibrina.
- Estas interacciones explican la paradoja entre los hallazgos epidemiológicos y los efectos in vitro del factor XIII 34Leu.
- Es probable que las interacciones gen-gen y gen-ambiente contribuyan a la complejidad del riesgo cardiovascular.
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