The δ-Opioid Receptor Affects Epidermal Homeostasis via ERK-Dependent Inhibition of Transcription Factor POU2F3.

Détails

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Etat: Serval
Version: de l'auteur
ID Serval
serval:BIB_BD7FD07B16AF
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
The δ-Opioid Receptor Affects Epidermal Homeostasis via ERK-Dependent Inhibition of Transcription Factor POU2F3.
Périodique
Journal of Investigative Dermatology
Auteur(s)
Neumann C., Bigliardi-Qi M., Widmann C., Bigliardi P.L.
ISSN
1523-1747 (Electronic)
ISSN-L
0022-202X
Statut éditorial
Publié
Date de publication
2015
Peer-reviewed
Oui
Volume
135
Numéro
2
Pages
471-480
Langue
anglais
Notes
Publication types: Journal Article Publication Status: ppublish
Résumé
Neuropeptides and their receptors are present in human skin, and their importance for cutaneous homeostasis and during wound healing is increasingly appreciated. However, there is currently a lack of understanding of the molecular mechanisms by which their signaling modulates keratinocyte function. Here, we show that δ-opioid receptor (DOPr) activation inhibits proliferation of human keratinocytes, resulting in decreased epidermal thickness in an organotypic skin model. DOPr signaling markedly delayed induction of keratin intermediate filament (KRT10) during in vitro differentiation and abolished its induction in the organotypic skin model. This was accompanied by deregulation of involucrin (IVL), loricrin, and filaggrin. Analysis of the transcription factor POU2F3, which is involved in regulation of KRT10, IVL, and profilaggrin expression, revealed a DOPr-mediated extracellular signal-regulated kinase (ERK)-dependent downregulation of this factor. We propose that DOPr signaling specifically activates the ERK 1/2 mitogen-activated protein kinase pathway to regulate keratinocyte functions. Complementing our earlier studies in DOPr-deficient mice, these data suggest that DOPr activation in human keratinocytes profoundly influences epidermal morphogenesis and homeostasis.
Pubmed
Web of science
Open Access
Oui
Création de la notice
07/02/2015 14:55
Dernière modification de la notice
09/05/2019 0:33
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