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Catenin dislocation in oral pemphigus vulgaris
Author(s) -
Mignogna Michele Davide,
Pan Giuseppe,
Muzio Lorenzo,
Staibano Stefania,
Bucci Eduardo
Publication year - 2001
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1034/j.1600-0714.2001.300503.x
Subject(s) - acantholysis , catenin , pemphigus vulgaris , cadherin , pathogenesis , cell adhesion molecule , pathology , microbiology and biotechnology , immunohistochemistry , beta catenin , medicine , chemistry , cell , biology , immunology , antibody , signal transduction , biochemistry , autoantibody , wnt signaling pathway
Cell‐to‐cell adhesion is mediated by cadherins (integral membrane proteins), which form a complex with catenins (cytoplasmatic proteins). While E‐cadherin expression has been extensively studied in many human skin diseases, less is known about the expression levels of catenins in oral blistering diseases. The purpose of this study was to evaluate the role of these proteins in the pathogenesis of acantholysis in oral pemphigus vulgaris. We evaluated by immunohistochemistry beta‐ and gamma‐catenin expression in 7 cases of oral pemphigus vulgaris (PV) at various stages of the disease and, as controls, in 18 healthy patients. Healthy cases showed, as reported in the literature, a strong reactivity with both beta‐ and gamma‐catenins, with the intensity of staining progressively decreasing from the spinous to the keratinised layers of epithelium, which had a prevalent cellular membrane expression. In PV patients, we detected a loss of membrane expression of these molecules with a progressive displacement of the signal toward the cytosol and, for gamma‐catenin, nuclear dislocation, particularly in areas with intense acantholysis.