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• W2914821421 abstract "Au regard des agressions environnementales constantes que la peau doit endurer, l'equilibre fragile entre l'expression et la repression des genes epidermiques, necessaire a la differentiation et la proliferation des keratinocytes, pourrait facilement etre perturbe en l'absence des mecanismes de stabilisation robustes. La presence d'un systeme neuroendocrinien local est donc importante afin de coordonner une reponse aux eventuelles irritations. En effet, l'expression de plusieurs neurohormones, des neurotransmetteurs et des neuropeptides, y compris des derives pro-opiomelanocortine comme la s-endorphine et [Met5]-enkephaline, ainsi que l'expression du recepteur 8-opioide (DOR) a ete demontre dans la peau. Cependant, les mecanismes moleculaires par lesquels ils modulent la fonction des keratinocytes sont mal connus.Le present travail demontre que la voie de signalisation DOR active specifiquement la voie ERK 1/2 MAPK dans les lignees cellulaires de keratinocytes humains, inhibant la proliferation des cellules et entraine une diminution de l'epaisseur epidermique dans un modele organotypique de peau. De plus, l'expression de DOR retarde nettement l'induction de la keratine 10 (KRT 10) et la keratine 1 (KRT 1) dans une modele 2D de differentiation in vitro, et supprime l'induction de KRT 10 dans un modele organotypique de peau. Ceci est accompagne de la deregulation de l'involucrine (IVL), la loricrine (LOR) et la filaggrin (FLG), resultant en une induction nettement reduite de leur expression lors de l'initiation de la differentiation in vitro.De plus, POU2F3 a ete identifie comme un facteur de transcription regulant les genes de differentiation des keratinocytes modules par DOR. Il a ete demontre que la regulation negative de POU2F3 via la voie DOR-ERK affecte les principaux aspects de la fonction des keratinocytes. Toutefois, il est evident que des facteurs supplementaires influencent la fonctionnalite de la voie DOR elle-meme. Le calcium et le contact cellule-cellule augmentent la quantite des recepteurs a la surface cellulaire des keratinocytes. Les keratinocytes dont les recepteurs sont internalises ne repondent pas de la meme maniere que ceux possedant des recepteurs fonctionnels localisee a la membrane.Ce travail suggere que lors de signaux intrinseques ou extrinseques specifiques, les keratinocytes sont capable de repondre via le systeme opioidergique neuro-epidermique. Cette reponse doit etre spatialement et temporairement controlee afin d'eviter un desequilibre de l'homeostasie epidermique et un retard de cicatrisation. La comprehension de ce processus tres complexe pourrait permettre a terme le developpement de meilleurs traitements des affections cutanees pathologiques. En complement des etudes precedentes sur des souris DOR-deficientes, ces donnees suggerent que l'activation de DOR dans les keratinocytes humains influence la morphogenese et l'homeostasie de l'epiderme, et pourrait jouer un role lors du processus de cicatrisation.-In view of the constant environmental assaults that the skin must endure, the delicate balance of an eloquent sequence of epidermal gene expression and repression, that is required for appropriate differentiation and proliferation of keratinocytes, might easily become derailed in the absence of robust stabilizing mechanisms. The presence of a local neuroendocrine system is thereby important to coordinate a response towards irritations. In fact, the expression of several neurohormones, neurotransmitters, and neuropeptides, including proopiomelanocortin derivatives, such as s- endorphin and [Met5]-enkephalin has been shown in skin, as well as expression of the 6-opioid receptor (DOR). However, there is currently a lack of understanding of the molecular mechanisms by which their signalling modulates keratinocyte function.The present work demonstrates that DOR signalling specifically activates the ERK 1/2 MAPK pathway in human keratinocyte cell lines. This activation inhibits cell proliferation, resulting in decreased epidermal thickness in an organotypic skin model. Furthermore, DOR expression markedly delays induction of keratin intermediate filament Keratin 10 (KRT 10) and KRT 1 during in vitro differentiation, and abolishes the induction of KRT 10 in the organotypic skin model. This is accompanied by deregulation of involucrin (IVL), loricrin (LOR), and filaggrin (FLG), illustrated by a markedly reduced induction of their expression upon initiation of differentiation in vitro. Additionally, POU2F3 was identified as a transcription factor mediating the DOR induced regulation of keratinocyte differentiation related genes. It was revealed that DOR-mediated ERK-dependent downregulation of this factor affects key aspects of keratinocyte function.However, it is evident that additional triggers influence the functionality of the DOR itself. Calcium at concentrations above 0.1 mM and cell-cell contact both enhance the presence of receptor molecules on the keratinocytes cell surface. Keratinocytes with internalized receptor do not respond to DOR ligands in the same way as keratinocytes with a functional membrane localized receptor." @default.
• W2914821421 created "2019-02-21" @default.
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• W2914821421 date "2013-01-01" @default.
• W2914821421 modified "2023-09-26" @default.
• W2914821421 title "The role of the δ-opioid receptor in skin homeostasis and wound healing" @default.
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