Inverse relationship between increased apoptosis and decreased skin cancer in UV-irradiated CD1d-/- mice

Détails

ID Serval
serval:BIB_61510E62BE1F
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Inverse relationship between increased apoptosis and decreased skin cancer in UV-irradiated CD1d-/- mice
Périodique
Photochemistry and Photobiology
Auteur(s)
Matsumura  Y., Moodycliffe  A. M., Nghiem  D. X., Ullrich  S. E., Ananthaswamy  H. N.
ISSN
0031-8655 (Print)
Statut éditorial
Publié
Date de publication
02/2005
Volume
81
Numéro
1
Pages
46-51
Notes
Journal Article --- Old month value: Jan-Feb
Résumé
We previously demonstrated that CD1d knockout mice were resistant to ultraviolet (UV)-induced immunosuppression. Because immune suppression is a critical factor in the development of UV-induced skin cancers, we investigated the response of wild type (WT) and CD1d-/- mice to UV carcinogenesis. We found that although 100% of WT mice developed skin tumors after 45 weeks of UV irradiation, only 60% of CD1d-/- mice developed skin tumors. To investigate the mechanisms involved in the resistance of CD1d-/- mice to UV-induced carcinogenesis, we determined the time course and kinetics of keratinocyte cell death after UV irradiation. After acute UV exposure, the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL)-positive keratinocytes were eliminated from the skin of WT mice by 72 h post-UV, but they still persisted until 96 h in CD1d-/- mice. The kinetics of p53 protein expression closely followed the kinetics of apoptotic cell death. Chronic UV irradiation resulted in induction of a significantly higher number of apoptotic keratinocytes in CD1d-/- than WT mice. In addition, epidermis and dermis from chronically UV-irradiated CD1d-/- mice harbored significantly fewer p53 mutations than WT mice. These results indicate that the resistance of CD1d-/- mice to UV carcinogenesis may be due to increased cell death and elimination of keratinocytes and fibroblasts containing DNA damage and p53 mutations.
Mots-clé
Animals Antigens, CD1/genetics/*physiology *Apoptosis Genes, p53 Mice Mice, Knockout Mutation Neoplasms, Radiation-Induced/genetics/*pathology Skin Neoplasms/genetics/*pathology *Ultraviolet Rays
Pubmed
Web of science
Création de la notice
25/01/2008 17:50
Dernière modification de la notice
20/08/2019 15:18
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