Order and disorder in corneocyte adhesion

Abstract

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.

Control of the Physical and Antimicrobial Skin Barrier by an IL-31–IL-1 Signaling Network

“…Most notably, the genes encoding desmoglein 1 and 4 but also desmocollin 1 and 2 and corneodesmosin were downregulated. Desmoglein 1 and desmocollin 1 are essential components of corneodesmosomes and targets of proteases important for skin desquamation (1,(56)(57)(58). Corneodesmosin is covalently linked to the cornified envelope (6,59).…”

Etanercept restores a differentiated keratinocyte phenotype in psoriatic human skin: a morphological study

“…Upregulation of keratin (K) isoforms produced by hyperplastic keratinocytes, K6/K16 (1), downregulation of K1/K10 (2), over-expression of K14 isoform (2) and atypical localisation of involucrin (3) were observed in psoriasis. Significant studies analysed the distribution of tight junctions (TJs) (4)(5)(6)(7)(8)(9), adherens junctions (AJs) (6,9,10), gap junctions (GJs) (11)(12)(13) and corneodesmosomes (14)(15)(16) in psoriasis.…”

Current Genetics in Hair Diseases

“…One of the major components of the corneodesmosome is corneodesmosin (CDSN). CDSN is secreted by cytoplasmic vesicles into the extracellular core of desmosomes, and is progressively proteolysed by several serine proteases, such as kallikrein-related peptidases, which leads to the loss of cell-cell adhesivity in the SC and causes desquamation [42]. CDSN is also expressed predominantly in the IRS of the HF, and thus is considered to be important for terminal differentiation, as well as subsequent degradation of the IRS [43].…”