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La unión al factor de tejido del factor VII activado desencadena la proliferación de las células del músculo liso a
Plinio Cirillo1, Gaetano Calì, Paolo Golino
1Division of Cardiology, University of Naples Federico II, Italy.
Circulation
|June 3, 2004
Resumen
El factor VII (FVIIa) activado que se une al factor de tejido (TF) en las células del músculo liso desencadena la proliferación a través de una vía no coagulante, activando la cascada de señalización ERK.
Área de la Ciencia:
- Biología celular Biología celular.
- La bioquímica es la bioquímica.
- Biología vascular Biología vascular
Sus antecedentes:
- El factor de tejido (TF) inicia la coagulación, pero también puede actuar como un receptor celular.
- Se está investigando el papel de TF en la transducción de señales y la proliferación celular.
Objetivo del estudio:
- Para determinar si el factor VII (FVIIa) activado que se une a TF estimula la proliferación de las células del músculo liso (SMC).
- Para aclarar los mecanismos intracelulares involucrados en la proliferación de SMC inducida por FVIIa.
Principales métodos:
- Se evaluó la proliferación de SMC utilizando la incorporación de [3H]timidina y el recuento de células.
- Se utilizaron anticuerpos FVIIa inhibidos en el sitio activo (FVIIai) y anti-TF para investigar la especificidad.
- Se analizó la activación de la vía de la proteína activada por mitógeno (MAP) quinasa (ERK 1/2) p44/42 a través del Western blotting.
- Empleó un inhibidor de MEK (UO126) para confirmar el papel de la vía ERK.
Principales resultados:
- FVIIa indujo una proliferación de SMC dependiente de la dosis, que fue bloqueada por FVIIai y un anticuerpo anti-TF.
- La unión de FVIIa a TF activó la vía ERK 1/2, evidenciada por la fosforilación de ERK.
- La proliferación y la fosforilación de ERK fueron anuladas por el tratamiento con anticuerpos FVIIai o anti-TF.
- La inhibición de MEK suprimió la proliferación de SMC inducida por FVIIa, confirmando la participación de la vía ERK.
Conclusiones:
- FVIIa vinculante a TF en SMCs induce específicamente la proliferación a través de un mecanismo independiente de la coagulación.
- Esta interacción activa la vía de señalización ERK 1/2.
- Los hallazgos sugieren una nueva conexión entre la coagulación, la inflamación y la aterosclerosis.
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