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La p120-catenina media las respuestas inflamatorias en la piel
Mirna Perez-Moreno1, Michael A Davis, Ellen Wong
1Laboratory of Mammalian Cell Biology and Development, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10021, USA.
Cell
|February 14, 2006
Resumen
La pérdida de p120-catenina en la piel del ratón causa inflamación e hiperplasia epidérmica, no afectando las uniones de adherens, sino a través de la activación del factor nuclear kappa B (NFkB). Este estudio revela que el p120
Área de la Ciencia:
- Biología celular Biología celular.
- Dermatología Dermatología dermatología.
- Inmunología Inmunología.
Sus antecedentes:
- Se sabe que la p120-catenina estabiliza las uniones de adherens (AJ) en cultivos celulares.
- Los estudios in vivo en eucariotas inferiores no han establecido un papel para la p120-catenin.
- La función in vivo de la p120-catenina en la epidermis de los mamíferos sigue sin estar clara.
Objetivo del estudio:
- Para investigar la función in vivo de la p120-catenina en la epidermis del ratón.
- Para determinar las consecuencias de la deficiencia de p120-catenina en la homeostasis de la piel.
- Para dilucidar los mecanismos moleculares subyacentes al papel de la p120-catenina en la regulación epidérmica.
Principales métodos:
- La orientación del gen condicional en ratones para crear la epidermis nula p120.
- Análisis de la estructura epidérmica, la función de barrera y la adhesión intercelular.
- Experimentos de injerto de piel y tratamiento con fármacos antiinflamatorios.
- Evaluación in vitro e in vivo de la activación del factor nuclear kappa B (NFkB).
- Investigación de la regulación de la Rho GTPasa por el p120-catenin.catenin.
Principales resultados:
- La epidermis nula neonatal p120 mostró componentes AJ reducidos pero la función de barrera intacta.
- Envejecimiento p120 ratones nulos desarrollaron hiperplasia epidérmica, inflamación crónica, degeneración del cabello y pérdida de grasa.
- Estos fenotipos estaban vinculados a la activación de NFkB, no a las proteínas de unión reducidas.
- p120 células epidermáticas nulas exhibieron activación nuclear de NFkB y objetivos inflamatorios aguas abajo.
- La p120-catenina influye en la activación de NFkB y la homeostasis inmune, en parte a través de las Rho GTPasas.
Conclusiones:
- La p120-catenina juega un papel crítico in vivo en el mantenimiento de la homeostasis inmunológica de la piel.
- La deficiencia epidérmica de p120-catenina conduce a la inflamación y hiperplasia impulsadas por NFkB.
- La regulación de las Rho GTPasas es un mecanismo clave por el cual la p120-catenina impacta las respuestas inmunes en la piel.
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