Premium
Order and disorder in corneocyte adhesion
Author(s) -
ISHIDAYAMAMOTO Akemi,
IGAWA Satomi,
KISHIBE Mari
Publication year - 2011
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/j.1346-8138.2011.01227.x
Subject(s) - desquamation , stratum corneum , corneocyte , atopic dermatitis , psoriasis , desmoglein 1 , dermatology , desmosome , staphylococcal scalded skin syndrome , epidermis (zoology) , chemistry , microbiology and biotechnology , biology , medicine , pathology , cell , anatomy , biochemistry , genetics , disease , autoimmune disease , bacteria , staphylococcus aureus
Epidermal cornified cells are attached to each other with modified desmosomes, namely corneodesmosomes. Changes in the corneodesmosome degradation process influence the total thickness of the stratum corneum and surface appearance of the skin. The major extracellular constituents of corneodesmosomes are desmoglein 1, desmocollin 1 and corneodesmosin. The intracellular part of corneodesmosomes is cross‐linked into cornified cell envelopes. Corneodesmosomes are degraded from the central surface area of each cell. Peripheral corneodesmosomes retain structural integrity up to the skin surface. A hypothesis where tight junctions in the stratum corneum play a role in this spatial difference in corneodesmosome degradation has recently been proposed. Genetic defects in corneodesmosin and inhibitors for proteases involved in corneodesmosome degradation result in accelerated desquamation and severe barrier impairment, presenting as the inflammatory type of peeling skin syndrome and Netherton syndrome, respectively. Abnormal corneodesmosome degradation is also found in more common skin diseases including ichthyosis vulgaris, atopic dermatitis, psoriasis vulgaris, lichen planus and soap‐induced xerosis.