Fiche publication
Date publication
février 2018
Journal
Photochemistry and photobiology
Auteurs
Membres identifiés du Cancéropôle Est :
Pr HUMBERT Philippe
Tous les auteurs :
Nakyai W, Tissot M, Humbert P, Grandmottet F, Viyoch J, Viennet C
Lien Pubmed
Résumé
Skin photoaging is caused by cumulative UVA exposure that leads to dermal matrix alterations associated with impaired fibroblast functions. In this study, we evaluated the effects of repeated UVA irradiation on mechanically stressed fibroblasts which were embedded in 3D tense collagen matrix. By comparison to 2D monolayer culture, we investigated the expressions of alpha-smooth muscle actin (α-SMA) cytoskeleton and α2 subunit of integrin receptors, as well as the collagen metabolism, focusing to MMP-1 and collagen type-I expressions. We found that UVA exposure reduces collagen levels in both culture conditions. However, concerning integrin α2 and α-SMA expression, UVA irradiation had no effect on 2D culture, whereas in tense 3D culture, it had an inhibitory effect. In UVA-irradiated 3D culture, fibroblasts acquired elongated shape and lost their dynamic interaction with collagen fibers through a decrease in integrin α2 and α-SMA. Fibroblast responses to UVA irradiation were different in 2D versus 3D environment, highlighting the importance of collagen environment in the regulation of mechanical activities. The behavior of fibroblast upon mechanical stimulation closely mimics stressed extracellular environment. The model of UVA-irradiated fibroblasts cultured in tense 3D collagen gel illustrated the in vivo situation of both mechanically stressed and photoaged human skin.
Mots clés
Actins, metabolism, Cell Culture Techniques, Cell Cycle, radiation effects, Cells, Cultured, Collagen Type I, genetics, Female, Fibroblasts, enzymology, Humans, Integrin alpha2, metabolism, Matrix Metalloproteinase 1, genetics, Middle Aged, RNA, Messenger, genetics, Skin, cytology, Skin Aging, radiation effects, Tissue Scaffolds, Ultraviolet Rays
Référence
Photochem. Photobiol.. 2018 Feb 8;:
