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Desmoglein isoform distribution affects stratum corneum structure and function.
P M Elias1, N Matsuyoshi, H Wu
1Department of Dermatology, University of California San Francisco, San Francisco, California 94143, USA.
The Journal of Cell Biology
|April 20, 2001
Summary
Altering desmoglein 3 distribution in mouse epidermis disrupts the skin barrier, causing dehydration and scaling. This highlights desmoglein
Area of Science:
- Cell biology
- Dermatology
- Molecular biology
Background:
- Desmogleins are key cell-cell adhesion molecules in stratified squamous epithelia.
- Two major isoforms, desmoglein 1 and desmoglein 3, have distinct distributions in epidermis and mucous membranes.
- The functional significance of this differential distribution remains unclear.
Purpose of the Study:
- To investigate the functional role of desmoglein isoform distribution in epidermal barrier formation.
- To determine how altering desmoglein 3 localization impacts epidermal structure and function.
Main Methods:
- Engineered transgenic mice to express desmoglein 3 under the involucrin promoter, mimicking mucous membrane distribution in epidermis.
- Analyzed epidermal morphology, differentiation markers, and stratum corneum structure.
- Assessed transepidermal water loss (TEWL) using in vitro and in vivo methods and tape stripping.
Main Results:
- Transgenic mice exhibited altered desmoglein 3 distribution in the epidermis.
- Epidermal stratum corneum showed abnormal lamellar structure and premature corneocyte loss.
- Mice displayed increased TEWL, severe dehydration, and died shortly after birth.
- Tape stripping confirmed premature corneocyte dysadhesion.
Conclusions:
- Differential desmoglein isoform expression is critical for epidermal barrier integrity.
- Altering desmoglein 3 distribution disrupts stratum corneum cohesion, leading to excessive water loss.
- Desmoglein isoform localization significantly impacts the permeability barrier function of the epidermis.