BMP-2 and TGF-beta1 differentially control expression of type II procollagen and alpha 10 and alpha 11 integrins in mouse chondrocytes.

Détails

ID Serval
serval:BIB_CF9CEC66FA9A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
BMP-2 and TGF-beta1 differentially control expression of type II procollagen and alpha 10 and alpha 11 integrins in mouse chondrocytes.
Périodique
European Journal of Cell Biology
Auteur(s)
Gouttenoire J., Bougault C., Aubert-Foucher E., Perrier E., Ronzière M.C., Sandell L., Lundgren-Akerlund E., Mallein-Gerin F.
ISSN
1618-1298[electronic], 0171-9335[linking]
Statut éditorial
Publié
Date de publication
2010
Volume
89
Numéro
4
Pages
307-314
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Bone morphogenetic protein (BMP)-2 and transforming growth factor (TGF)-beta1 are multifunctional cytokines both proposed as stimulants for cartilage repair. Thus it is crucial to closely examine and compare their effects on the expression of key markers of the chondrocyte phenotype, at the gene and protein level. In this study, the expression of alpha 10 and alpha 11 integrin subunits and the IIA/IIB spliced forms of type II procollagen have been monitored for the first time in parallel in the same in vitro model of mouse chondrocyte dedifferentiation/redifferentiation. We demonstrated that TGF-beta1 stimulates the expression of the non-chondrogenic form of type II procollagen, IIA isoform, and of a marker of mesenchymal tissues, i.e. the alpha 11 integrin subunit. On the contrary, BMP-2 stimulates the cartilage-specific form of type II procollagen, IIB isoform, and a specific marker of chondrocytes, i.e. the alpha 10 integrin subunit. Collectively, our results demonstrate that BMP-2 has a better capability than TGF-beta1 to stimulate chondrocyte redifferentiation and reveal that the relative expressions of type IIB to type IIA procollagens and alpha 10 to alpha 11 integrin subunits are good markers to define the differentiation state of chondrocytes. In addition, adenoviral expression of Smad6, an inhibitor of BMP canonical Smad signaling, did not affect expression of total type II procollagen or the ratio of type IIA and type IIB isoforms in mouse chondrocytes exposed to BMP-2. This result strongly suggests that signaling pathways other than Smad proteins are involved in the effect of BMP-2 on type II procollagen expression.
Mots-clé
Animals, Bone Morphogenetic Protein 2/metabolism, Cell Differentiation, Cells, Cultured, Chondrocytes/metabolism, Collagen Type II/biosynthesis, Integrin alpha Chains/biosynthesis, Mice, Procollagen/biosynthesis, Transforming Growth Factor beta1/metabolism
Pubmed
Web of science
Création de la notice
02/02/2011 16:52
Dernière modification de la notice
20/08/2019 16:50
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