Nuclear factor I-C links platelet-derived growth factor and transforming growth factor beta1 signaling to skin wound healing progression.

Détails

ID Serval
serval:BIB_009622F1FEE9
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Nuclear factor I-C links platelet-derived growth factor and transforming growth factor beta1 signaling to skin wound healing progression.
Périodique
Molecular and Cellular Biology
Auteur(s)
Plasari G., Calabrese A., Dusserre Y., Gronostajski R.M., McNair A., Michalik L., Mermod N.
ISSN
1098-5549[electronic], 0270-7306[linking]
Statut éditorial
Publié
Date de publication
2009
Peer-reviewed
Oui
Volume
29
Numéro
22
Pages
6006-6017
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Transforming growth factor beta (TGF-beta) and platelet-derived growth factor A (PDGFAlpha) play a central role in tissue morphogenesis and repair, but their interplay remain poorly understood. The nuclear factor I C (NFI-C) transcription factor has been implicated in TGF-beta signaling, extracellular matrix deposition, and skin appendage pathologies, but a potential role in skin morphogenesis or healing had not been assessed. To evaluate this possibility, we performed a global gene expression analysis in NFI-C(-/-) and wild-type embryonic primary murine fibroblasts. This indicated that NFI-C acts mostly to repress gene expression in response to TGF-beta1. Misregulated genes were prominently overrepresented by regulators of connective tissue inflammation and repair. In vivo skin healing revealed a faster inflammatory stage and wound closure in NFI-C(-/-) mice. Expression of PDGFA and PDGF-receptor alpha were increased in wounds of NFI-C(-/-) mice, explaining the early recruitment of macrophages and fibroblasts. Differentiation of fibroblasts to contractile myofibroblasts was also elevated, providing a rationale for faster wound closure. Taken together with the role of TGF-beta in myofibroblast differentiation, our results imply a central role of NFI-C in the interplay of the two signaling pathways and in regulation of the progression of tissue regeneration.
Mots-clé
Animals, Cell Differentiation, Cell Movement, Cells, Cultured, Embryo, Mammalian/cytology, Extracellular Matrix/genetics, Extracellular Matrix Proteins/metabolism, Fibroblasts/cytology, Fibroblasts/metabolism, Gene Deletion, Gene Expression Regulation, Macrophages/cytology, Mice, Mice, Knockout, NFI Transcription Factors/deficiency, NFI Transcription Factors/metabolism, Oligonucleotide Array Sequence Analysis, Platelet-Derived Growth Factor/metabolism, Reproducibility of Results, Signal Transduction, Skin/metabolism, Skin/pathology, Transforming Growth Factor beta1/metabolism, Wound Healing
Pubmed
Web of science
Open Access
Oui
Création de la notice
01/10/2009 11:06
Dernière modification de la notice
20/08/2019 12:22
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