Carrillo LM, Arciniegas CE, Rojas H, Ramírez R, Reyes O, Ortiz W

Idioma: Español
Referencias bibliográficas: 42
Paginas: 119-130
Archivo PDF: 1182.03 Kb.

RESUMEN

Introducción: La participación de algunas moléculas en la arquitectura y funcionamiento de la barrera epidérmica no ha sido completamente estudiada. Entre estas moléculas están desmogleína1, CD44, sindecan-1 y EGFR caracterizadas por presentar un N-terminal que posee cadenas laterales de glicanos, y galectina-3, un receptor de glicanos que contienen β-galactósidos. Objetivo: Examinar la distribución y localización de desmogleína1, CD44, sindecan-1, EGFR y galectina-3 en la epidermis normal y en la hiperplasia observada en liquen plano, placa psoriática y CBC. Material y métodos: Biopsias de pacientes diagnosticados con liquen plano, psoriasis vulgar y CBC (5 por cada patología) fueron seleccionadas. Seis muestras de piel normal también fueron examinadas. La distribución y locali­zación de desmogleína1, CD44, sindecan-1, EGFR y galectina-3 fue examinada por inmunofluorescencia usando un microscopio confocal. Resultados: En la epidermis normal desmogleína1, CD44, sindecan-1 y galectina-3 fueron detectadas en las capas superiores delineando los márgenes celulares y puentes entre queratinocitos adyacentes con un gradiente de expresión que aumentaba desde la capa basal hasta las capas suprabasales, mientras que en las epidermis hiperplásicas estaban restringidas a las capas suprabasales, apareciendo interrumpidas en los puentes entre muchos queratinocitos. Conclusiones: Nuestras observaciones sugieren que desmogleína1, CD44, sindecan-1 y EGFR a través de sus cadenas laterales de N- y O-glicanos podrían establecer asociaciones facilitadas por galectina-3, dando lugar a una red molecular que contribuiría al ensamble y estabilidad de los desmosomas en las capas superiores de la epidermis y que la perturbación de esta red podría dar lugar a una hiperplasia epidérmica.

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