Identification of Late Differentiation Antigens of Human Cornified Epithelia, Expressed in Re-Organized Desmosomes and Bound to Cross-Linked Envelope

Serre, Guy; Mils, Valérie; Haftek, Marek; Vincent, Christian; Croute, F.; Réano, A.; Ouhayoun, J.; Bettinger, Stéphane; Soleilhavoup, J.P.

doi:10.1111/1523-1747.ep12492589

Cited by 152 publications

(164 citation statements)

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“…These observations were compared with Cdsn expression in a range of other skin conditions. Both current and previously published results (Haftek et al 1997;Mils et al 1992;Serre et al 1991) suggest that in normal skin, synthesis and release of Cdsn is tightly controlled, with Cdsn synthesis occurring in the most superficial cells of the stratum granulosum and release of Cdsn restricted to the interface between stratum granulosum and stratum corneum. In psoriatic skin, contrasting with both normal skin and inflammatory skin conditions, such restricted control of Cdsn synthesis seems to be diminished, with widespread expression of Cdsn in multiple layers of stratum spinosum, and both cytoplasmic and cell surface expression.…”

Section: Discussionmentioning

confidence: 52%

“…Immunohistochemistry was performed using two monoclonal antibodies to Cdsn, G36-19 and F28-27 (Serre et al, 1991), which label different epitopes in the central domain of the Cdsn protein (Guerrin et al, 1998). Five-micron-thick sections were mounted on glass slides and either fixed in acetone (frozen tissue) or dewaxed in xylene and alcohol and microwave pretreated (paraffin-embedded tissue).…”

Section: Allen Et Almentioning

confidence: 99%

“…C orneodesmosin (Cdsn) is a late differentiation epidermal glycoprotein expressed in the stratum granulosum and stratum corneum of normal skin and thought to function as a keratinocyte adhesion molecule (Serre et al, 1991). Cdsn mRNA expression is restricted to keratinocytes of the granular layer in normal human epidermis (Zhou and Chaplin, 1993).…”

mentioning

confidence: 99%

“…In the stratum granulosum of normal skin, Cdsn is present as a 52 to 56 kd glycoprotein, whereas in the stratum corneum it exists as smaller macromolecules of 30 to 45 kd . Cdsn is initially observed intracellularly within keratinosomes and is then translocated to the cell surface, where it is incorporated into desmosomes, modifying them to corneodesmosomes (Serre et al, 1991). Some desmosomal proteins are important in maintaining keratinocyte cell-cell adhesion, and it is likely that Cdsn forms part of the adhesive network (Serre et al, 1991).…”

mentioning

confidence: 99%

“…Cdsn is initially observed intracellularly within keratinosomes and is then translocated to the cell surface, where it is incorporated into desmosomes, modifying them to corneodesmosomes (Serre et al, 1991). Some desmosomal proteins are important in maintaining keratinocyte cell-cell adhesion, and it is likely that Cdsn forms part of the adhesive network (Serre et al, 1991). Cdsn has a high glycine content, which implies a potential to form adhesive loop structures at the cell surface, as seen with other epidermal proteins (Guerrin et al, 1998).…”

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confidence: 99%

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Corneodesmosin Expression in Psoriasis Vulgaris Differs from Normal Skin and Other Inflammatory Skin Disorders

Allen

Ishida‐Yamamoto

McGrath

et al. 2001

Laboratory Investigation

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SUMMARY:Corneodesmosin (Cdsn) is a late differentiation epidermal glycoprotein putatively involved in keratinocyte adhesion.The Cdsn gene lies within the susceptibility region on chromosome 6p21.3 (PSORS1) for psoriasis, a common chronic disfiguring skin disease. A particular allelic variant of Cdsn has a strong association with psoriasis. Therefore, genetically and biologically, Cdsn is a possible candidate gene for psoriasis susceptibility. To investigate a potential role for Cdsn in psoriasis pathogenesis, protein expression studies were performed by quantitative immunohistochemistry on normal skin, psoriatic skin (lesional and nonlesional), and other skin disorders using monoclonal antibodies (G36-19 and F28-27). In normal and nonlesional skin, Cdsn was expressed in stratum corneum and one or two layers of superficial stratum granulosum. In lesional psoriasis, there was a significant increase in Cdsn expression, which was observed in multiple layers of stratum spinosum and in stratum corneum. The expression pattern varied from granular, cytoplasmic immunoreactivity to cell surface labeling with weakly immunoreactive cytoplasm. In chronic atopic dermatitis, lichen planus, mycosis fungoides, and pityriasis rubra pilaris, Cdsn immunoreactivity was confined to stratum corneum and upper stratum granulosum with no stratum spinosum immunoreactivity. Immunoelectron microscopy of normal and lesional psoriatic skin demonstrated Cdsn release concomitant with involucrin incorporation into cell envelopes and completed before mature envelope formation. Extracellular release of Cdsn occurred at a lower level of the epidermis in psoriasis than normal skin. These protein expression studies provide evidence of altered Cdsn expression in psoriasis consistent with a role of Cdsn in disease pathogenesis. Further functional and genetic studies of Cdsn are justified to determine its role as a potential psoriasis-susceptibility factor. (Lab Invest 2001, 81:969 -976).

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Section: Discussionmentioning

confidence: 52%

Section: Allen Et Almentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Corneodesmosin Expression in Psoriasis Vulgaris Differs from Normal Skin and Other Inflammatory Skin Disorders

Allen

Ishida‐Yamamoto

McGrath

et al. 2001

Laboratory Investigation

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Stratum corneum, corneodesmosomes and ex vivo percutaneous penetration

Haftek

Teillon

Schmitt

1998

Microsc. Res. Tech.

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Cornification of the Skin: A Non‐apoptotic Cell Death Mechanism

Candi

Knight

Melino

2009

Encyclopedia of Life Sciences

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The most important function of the epidermis is to form a barrier against the environment by means of several layers of terminally differentiated, dead keratinocytes, the cornified envelope (CE). CEs consist of keratins enclosed within an insoluble amalgam of proteins and lipids. Transglutaminase enzymes catalyse the formation of characteristic crosslinks between structural proteins to form the protein part of the CE. Another form of cell death, that is, apoptosis, which has a completely different molecular mechanism and physiological significance, also occurs in the skin. Defects of apoptosis are related to the development of cancer, whereas CE abnormalities are associated with barrier abnormalities and ichthyosis. Key concepts: Keratinocyte apoptosis (occurring in basal layer) is an active and rapid, energy‐dependent, gene‐directed biochemical pathway of defensive cell death that does not require de novo protein synthesis and preserves plasma membrane. Cornification, the keratinocyte differentiation programme (occurring in upper layer), is a slow, coordinated process in space and time, which allows the formation of a layer of dead cells (corneocytes) to create a physical barrier for the skin. The stratum corneum is composed of tightly attached corneocytes with mostly keratin intermediate filaments (KIFs) embedded into a filaggrin matrix. The structural proteins of the CE, including involucrin, loricrin, trichohyalin and the class of small proline‐rich proteins (SPRs), constitute about 7–10% of the mass of the epidermis. These structural proteins together with lipids (ceramides) form the complete barrier. Transglutaminase are Ca 2+ ‐dependent enzymes that catalyse the formation of N ε ‐(γ‐glutamyl)lysine bonds between CE structural proteins to confer the characteristic resistance and insolubility to the skin. The junctions responsible for intercellular adhesion and for cohesion of the stratum corneum of the epidermis are of two types: (1) the adherence junctions (connecting the actin cytoskeleton of neighbouring cells) and (2) desmosomes (connecting the keratin filament cytoskeleton of adjacent cells). Proteases are involved in at least three processes in skin differentiation. First, certain cornified envelope precursors require proteolytic processing before cornified envelope formation occurs. Second, the loss of nuclei and mitochondria requires proteolytic processing. Third, desquamation requires proteolysis of the corneodesmosomes.

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Identification of Late Differentiation Antigens of Human Cornified Epithelia, Expressed in Re-Organized Desmosomes and Bound to Cross-Linked Envelope

Cited by 152 publications

References 53 publications

Corneodesmosin Expression in Psoriasis Vulgaris Differs from Normal Skin and Other Inflammatory Skin Disorders

Corneodesmosin Expression in Psoriasis Vulgaris Differs from Normal Skin and Other Inflammatory Skin Disorders

Stratum corneum, corneodesmosomes and ex vivo percutaneous penetration

Cornification of the Skin: A Non‐apoptotic Cell Death Mechanism

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