The aryl hydrocarbon receptor mediates UVB radiation-induced skin tanning.
J Invest Dermatol
; 131(1): 203-10, 2011 Jan.
Article
de En
| MEDLINE
| ID: mdl-20861855
ABSTRACT
Melanogenesis is the vital response to protect skin cells against UVB-induced DNA damage. Melanin is produced by melanocytes, which transfer it to surrounding keratinocytes. Recently, we have shown that the aryl hydrocarbon receptor (AhR) is part of the UVB-stress response in epidermal keratinocytes. UVB triggers AhR signaling by generating the AhR ligand 6-formylindolo(3,2-b)carbazole from tryptophan. We show here that normal murine melanocytes express functional AhR. Using standard UVB tanning protocols, AhR-deficient mice were shown to tan significantly weaker than wild-type mice; in these mice, tyrosinase activity in the epidermis was lower as well. Tanning responses and tyrosinase activity, however, were normal in keratinocyte-specific conditional AhR knockout mice, indicating that release of melanogenic keratinocyte factors is unaffected by the UVB-AhR signaling pathway and that the diminished tanning response in AhR(-/-) mice is confined to the level of melanocytes. Accordingly, the number of dihydroxyphenylalanin-positive melanocytes increased significantly less on UVB irradiation in AhR(-/-) mice than in wild-type mice. This difference in melanocyte number was associated with a significantly reduced expression of stem cell factor-1 and c-kit in melanocytes of AhR(-/-) mice. Thus, the environmental signal sensor AhR links solar UVB radiation to skin pigmentation.
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Rayons ultraviolets
/
Pigmentation de la peau
/
Récepteurs à hydrocarbure aromatique
/
Mélanocytes
Limites:
Animals
Langue:
En
Journal:
J Invest Dermatol
Année:
2011
Type de document:
Article
Pays d'affiliation:
Allemagne