Titre
Coactivation of AP-1 activity and TGF-beta1 gene expression in the stress response of normal skin cells to ionizing radiation.
Type
article
Institution
Externe
Périodique
Auteur(s)
Martin, M.
Auteure/Auteur
Vozenin, M.C.
Auteure/Auteur
Gault, N.
Auteure/Auteur
Crechet, F.
Auteure/Auteur
Pfarr, C.M.
Auteure/Auteur
Lefaix, J.L.
Auteure/Auteur
Liens vers les personnes
ISSN
0950-9232
Statut éditorial
Publié
Date de publication
1997-08-18
Volume
15
Numéro
8
Première page
981
Dernière page/numéro d’article
989
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Résumé
Activation of the AP-1 transcription factor and TGF-beta1 growth factor by ionizing radiation was studied both in vivo in pig skin, and in vitro in human fibroblasts and keratinocytes. Three and 6 h after irradiation, the Fos and Jun proteins and their binding activity to an AP-1 consensus sequence were strongly induced by high doses of gamma-rays. c-Fos, c-Jun and JunB proteins were found to be present in gel-shift complexes by probing with specific antibodies. Both keratinocytes and fibroblasts exhibited heightened AP-1 activity following irradiation. As we previously found that TGF-beta1 is involved in the development of skin lesions induced by radiation, TGF-beta1 gene expression was also examined. Two and 6 h after irradiation, the levels of TGF-beta1 transcripts were increased in skin. By immunostaining, TGF-beta1 protein levels were found to be increased in fibroblasts, keratinocytes and endothelial cells. As the TGF-beta1 promoter contains AP-1 binding sites, the relation between AP-1 activity and TGF-beta1 induction was addressed. The -365 TGF-beta1 promoter fragment, which contains a high affinity AP-1 site, exhibited increased binding to Jun and Fos proteins following irradiation. These results suggest that stress-inducible TGF-beta1 expression is mediated by the activation of AP-1 transcription factor.
PID Serval
serval:BIB_231B6FD88EBC
PMID
Open Access
Oui
Date de création
2018-04-27T14:02:42.632Z
Date de création dans IRIS
2025-05-20T16:45:32Z