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Activation of canonical Wnt signalling is required for TGF-β-mediated fibrosis
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Activation of canonical Wnt signalling is required for TGF-β-mediated fibrosis
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Journal Article
Activation of canonical Wnt signalling is required for TGF-β-mediated fibrosis
2012
Overview
The transforming growth factor-β (TGF-β) signalling pathway is a key mediator of fibroblast activation that drives the aberrant synthesis of extracellular matrix in fibrotic diseases. Here we demonstrate a novel link between transforming growth factor-β and the canonical Wnt pathway. TGF-β stimulates canonical Wnt signalling in a p38-dependent manner by decreasing the expression of the Wnt antagonist Dickkopf-1. Tissue samples from human fibrotic diseases show enhanced expression of Wnt proteins and decreased expression of Dickkopf-1. Activation of the canonical Wnt pathway stimulates fibroblasts
in vitro
and induces fibrosis
in vivo
. Transgenic overexpression of Dickkopf-1 ameliorates skin fibrosis induced by constitutively active TGF-β receptor type I signalling and also prevents fibrosis in other TGF-β-dependent animal models. These findings demonstrate that canonical Wnt signalling is necessary for TGF-β-mediated fibrosis and highlight a key role for the interaction of both pathways in the pathogenesis of fibrotic diseases.
Aberrant activation of the TGF-β pathway leads to fibrotic disease. Distler and colleagues show that TGF-β-mediated fibrosis requires the decrease of Dickkopf-1, an antagonist of canonical Wnt signalling, suggesting that the two pathways interact for the manifestation of this disease.
Publisher
Nature Publishing Group UK,Nature Pub. Group
Subject
/ 692/420
/ 692/699
/ Adult
/ Animals
/ Extracellular Matrix - metabolism
/ Female
/ Humanities and Social Sciences
/ Humans
/ Intercellular Signaling Peptides and Proteins - biosynthesis
/ Male
/ Mice
/ p38 Mitogen-Activated Protein Kinases - metabolism
/ Receptors, Transforming Growth Factor beta - metabolism
/ Science
