Cell death-induced activation of epidermal growth factor receptor in keratinocytes: implications for restricting epidermal damage in dermatitis.
Détails
Télécharger: BIB_DF547573566B.P001.pdf (1764.21 [Ko])
Etat: Public
Version: de l'auteur⸱e
Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_DF547573566B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Cell death-induced activation of epidermal growth factor receptor in keratinocytes: implications for restricting epidermal damage in dermatitis.
Périodique
Journal of Investigative Dermatology
ISSN
0022-202X (Print)
ISSN-L
0022-202X
Statut éditorial
Publié
Date de publication
2005
Volume
125
Numéro
1
Pages
134-142
Langue
anglais
Résumé
Recent findings have implicated Fas/Fas ligand (FasL) in mediating the death of keratinocytes in spongiotic lesions. We asked whether dying keratinocytes could potentially initiate a protective response of the skin to limit the destruction of the epidermis in the spongiotic areas. In addition to apoptosis, treatment of keratinocyte cultures in vitro with FasL triggers a profound phoshorylation of the epidermal growth factor receptor (EGFR) and of its downstream effectors ERK and protein kinase B (PKB/Akt). Using a variety of inhibitors and blocking antibodies, we demonstrated that: (i) apoptosis is required for the generation of the signal(s) leading to the activation of EGFR, ERK, and Akt; (ii) the activation of EGFR, ERK, and Akt by FasL is indeed mediated by its bona fide receptor Fas; (iii) the activation of EGFR is essential for the subsequent activation of ERK and Akt; and (iv) apoptotic keratinocytes secrete soluble EGFR ligands (including amphiregulin) that are processed from membrane-bound proligand forms by metalloproteinase(s). Our findings demonstrate a potential mechanism for the restriction and repair of spongiotic damage in eczemas.
Mots-clé
Apoptosis, Cell Culture Techniques, Dermatitis/metabolism, Dermatitis/pathology, Fas Ligand Protein, Humans, Keratinocytes/metabolism, Membrane Glycoproteins/metabolism, Receptor, Epidermal Growth Factor/metabolism, Signal Transduction
Pubmed
Web of science
Open Access
Oui
Création de la notice
19/01/2008 18:30
Dernière modification de la notice
20/08/2019 17:03