Increased expression of aquaporin 3 in atopic eczema.
Artikel i vetenskaplig tidskrift, 2006

BACKGROUND: Dry skin in atopic eczema depends on increased water loss. The mechanisms behind this are poorly understood. The aim of this work was to identify genes that may contribute to water loss in eczema. METHODS: Affymetrix DNA microarrays U133A were used to analyse gene expression in skin biopsies from 10 patients with atopic eczema and 10 healthy controls. RESULTS: DNA microarray analysis showed up-regulation of 262 genes and down-regulation of 129 genes in atopic eczema. The known functions of these genes were analysed using Gene Ontology to identify genes that could contribute to increased water loss. This led to identification of aquaporin 3 (AQP3), which has a key role in hydrating healthy epidermis. Increased expression of AQP3 was found in eczema compared with healthy skin. This was confirmed with real-time polymerase chain reaction (P<0.001). In healthy skin, epidermal AQP3 immunoreactivity was weak and mainly found in the stratum basale. A gradient was formed with decreasing AQP3 staining in the lower layers of the stratum spinosum. By contrast, in acute and chronic atopic eczema strong AQP3 staining was found in both the stratum basale and the stratum spinosum. CONCLUSIONS: Aquaporin 3 is the predominant aquaporin in human skin. Increased expression and altered cellular distribution of AQP3 is found in eczema and this may contribute to water loss.

Författare

Maja Olsson

Göteborgs universitet

Ann Broberg

Göteborgs universitet

Margareta Jernås

Göteborgs universitet

Lena M S Carlsson

Göteborgs universitet

Mats Rudemo

Göteborgs universitet

Chalmers, Matematiska vetenskaper, Matematisk statistik

Mark Suurküla

Göteborgs universitet

Per-Arne Svensson

Göteborgs universitet

Mikael Benson

Göteborgs universitet

Allergy: European Journal of Allergy and Clinical Immunology

0105-4538 (ISSN) 1398-9995 (eISSN)

Vol. 61 9 1132-7

Ämneskategorier

MEDICIN OCH HÄLSOVETENSKAP

DOI

10.1111/j.1398-9995.2006.01151.x

Mer information

Skapat

2017-10-06