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La activación de las células endoteliales por las estructuras formadoras de poros: papel fundamental para la
S Saadi1, R A Holzknecht, C P Patte
1Department of Surgery, Mayo Clinic, Rochester, MN 55905, USA. saadi.soheyla@mayo.edu
Circulation
|April 19, 2000
Resumen
El complejo de ataque de membrana del complemento (MAC) activa las células endoteliales (CE) a través de IL-1alfa, iniciando la inflamación. Este mecanismo es compartido por otras moléculas formadoras de poros, destacando una vía común para la activación celular.
Área de la Ciencia:
- Inmunología Inmunología.
- Biología celular Biología celular.
- Biología Vascular Biología Vascular
Sus antecedentes:
- La interacción del complemento con las células endoteliales (CE) impulsa la inflamación y la coagulación.
- El complejo de ataque de membrana (MAC) en ECs regula al alza el factor de tejido y la ciclooxigenasa-2 a través de IL-1alpha.
- Este estudio investiga si el MAC activa globalmente las EC a través de este mecanismo y si otras estructuras formadoras de poros lo utilizan.
Objetivo del estudio:
- Para determinar si el MAC activa globalmente las ECs porcina aórtica y microvascular.
- Para determinar si el mecanismo de activación de EC inducida por MAC es compartido por otras estructuras formadoras de poros.
- Para aclarar el papel de la IL-1alfa en la activación de la EC mediada por el complemento.
Principales métodos:
- Las EC fueron expuestas al complemento y la expresión génica (E-selectina, ICAM-1, VCAM-1, Ikappa-Balpha, IL-1alpha, IL-1beta, IL-8, PAI-1) fue analizada durante 6 horas.
- El antagonista del receptor IL-1 se utilizó para evaluar si la expresión génica era una respuesta primaria.
- Se emplearon anticuerpos anti-IL-1alfa para investigar el papel autocrino de la IL-1alfa.
- Se utilizaron péptidos formadores de poros (melittin, mastoparan) para estudiar su efecto sobre la inducción de la E-selectina.
Principales resultados:
- Complemento inducido por la regulación al alza de múltiples genes inflamatorios y relacionados con la coagulación en ECs.
- La expresión génica no fue una respuesta primaria, ya que el antagonista del receptor IL-1 la inhibió parcialmente.
- La activación de la EC mediada por el complemento dependía de la IL-1alfa autocrina, inhibida por los anticuerpos anti-IL-1alfa.
- Los péptidos formadores de poros melittin y mastoparan inducen la E-selectina a través de IL-1.
Conclusiones:
- Las proteínas formadoras de poros de transmembrana activan las EC a través de la señalización autocrina de la IL-1alfa.
- Esta vía es un mecanismo común para la activación de EC por diversas moléculas formadoras de poros.
- Los hallazgos sugieren un mecanismo unificado para el complemento y otros péptidos formadores de poros en la inflamación vascular.
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