The transmembrane
glycoprotein CD44 is currently thought to be the main
cell surface receptor for the
glycosaminoglycan hyaluronate. We previously showed that (1) CD44 regulate keratinocyte proliferation; (2) topical
retinoids dramatically increase the expression of CD44, hyaluronate and
hyaluronate synthase (HAS)s in mouse epidermis; (3) topical
retinaldehyde restores the epidermal thickness and CD44 expression which are correlated with clinical improvement in
lichen sclerosus et atrophicus lesions; and (4)
retinaldehyde-induced proliferative response of keratinocytes is a CD44-dependent phenomenon and requires the presence of
HB-EGF, erbB1 and
matrix metalloproteinases. In this study, we analyzed the effect of UV irradiation on the levels of epidermal hyaluronate and CD44 in mice, as well as its potential prevention by topical
retinoids. UVA (10 J/cm(2)) or UVB (1 J/cm(2)) irradiation significantly decreased the expression of CD44 and hyaluronate in the epidermis of hairless mice after 2 h. Expression of both epidermal CD44 and hyaluronate was reconstituted within 24 h. Topical application of
retinaldehyde for 3 days prior to UVA or UVB irradiation prevented the decrease of CD44 and hyaluronate expression. Topical
retinol and
retinoic acid also increased the basal levels of epidermal CD44 and hyaluronate, although their preventive effect on UV-induced decrease of these molecules was less pronounced as compared to topical
retinaldehyde. These data confirm the relationships between
retinoid and CD44 pathways, although the primary target(s) of UV leading to CD44 and hyaluronate degradation remain to be elucidated.