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El perfil de expresión génica de las células endotelial humanas inflamadas y la influencia de la proteína C activada
Nicola Franscini1, Esther B Bachli, Nenad Blau
1Medical Clinic B Research Unit, Department of Medicine, University Hospital, Zürich, Switzerland.
Circulation
|October 27, 2004
Resumen
La proteína C activada (APC) reduce la inflamación en las células endoteliales de la arteria coronaria humana mediante la regulación a la baja de los genes inflamatorios clave. Esta vía ofrece un nuevo mecanismo antiinflamatorio, particularmente eficaz en la inflamación leve a moderada.
Área de la Ciencia:
- Biología endotelial Biología endotelial
- Investigación de la inflamación en la investigación de la inflamación.
- Vías de la coagulación y la inflamación.
Sus antecedentes:
- La inflamación sistémica activa el endotelio vascular, causando hipotensión, trombosis y daño a los órganos.
- La vía de la proteína C activada (APC) vincula la coagulación y la inflamación.
- Las células endoteliales son fundamentales para las respuestas inflamatorias.
Objetivo del estudio:
- Para investigar los perfiles de expresión génica en las células endoteliales de la arteria coronaria humana (HCAEC) estimuladas con citoquinas proinflamatorias.
- Para determinar la influencia de la APC en la expresión de los genes candidatos regulados por estos estímulos.
Principales métodos:
- Las células endoteliales de la arteria coronaria humana (HCAEC) fueron estimuladas con interleucina-1beta, interferón-gamma y el factor de necrosis tumoral-alfa.
- Se realizó un perfil de expresión génica, seguido de una verificación utilizando PCR en tiempo real, ELISA y HPLC.
- Se evaluaron las actividades de los factores de transcripción.
Principales resultados:
- El APC regulaba a la baja la síntesis de tetrahidrobiopterina (BH4), la interleucina-6, la interleucina-8, la proteína quimiotáctica monocítica-1 (MCP-1) y la molécula de adhesión intercelular-1 (ICAM-1) en los niveles de transcripción y proteína.
- El APC inhibió las actividades de los factores de transcripción c-Fos, FosB y c-Rel en los HCAECs inflamados.
- El APC no afectó a la síntesis de óxido nítrico endotelial, a la molécula de adhesión endotelial o a la molécula de adhesión celular vascular-1.
Conclusiones:
- El APC exhibe un nuevo mecanismo antiinflamatorio en las HCAEC al suprimir la inducción c-Fos-dependiente de MCP-1 e ICAM-1.
- APC desregula la expresión y la actividad de los genes relacionados con la inflamación.
- Este efecto es más pronunciado bajo condiciones inflamatorias intermedias o leves.
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