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All-trans retinoic acid compromises desmosome expression in human epidermis
J D Humphries1, E J Parry, R E Watson
1Section of Dermatology, Department of Medicine, University of Manchester, Hope Hospital, Salford M6 8HD, U.K.
The British Journal of Dermatology
|January 20, 1999
Summary
Retinoid treatments like all-trans-retinoic acid (RA) can cause skin fragility by reducing desmosome expression in the epidermis. This compromises skin cohesion and leads to fragility.
Area of Science:
- Dermatology
- Cell Biology
- Biochemistry
Background:
- Skin fragility is a known side-effect of retinoid therapy.
- Desmosomes are crucial for maintaining the structural integrity and cohesion of epidermal keratinocytes.
Purpose of the Study:
- To investigate if all-trans-retinoic acid (RA) impacts desmosome expression in human epidermis.
- To determine if compromised desmosome expression contributes to retinoid-induced skin fragility.
Main Methods:
- Human volunteers received topical application of all-trans-retinoic acid (RA), sodium dodecyl sulphate (SDS), or vehicle.
- Skin biopsies were analyzed using immunofluorescence microscopy for desmosomal protein expression.
- Western blot analysis was performed to quantify desmocollin expression.
Main Results:
- Both RA and SDS treatments increased epidermal thickness compared to vehicle.
- RA and SDS equally reduced epidermal staining for desmoplakin, desmoglein 1, plakophilin 1, and desmocollin 3.
- RA caused a more significant reduction in desmocollin 1 compared to SDS, confirmed by Western blot.
Conclusions:
- All-trans-retinoic acid (RA) compromises desmosome expression in human epidermis.
- Reduced desmosomal adhesion due to decreased desmocollin expression likely contributes to retinoid-induced skin fragility.
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