Open Access Research article

Type-1 Collagen differentially alters β-catenin accumulation in primary Dupuytren's Disease cord and adjacent palmar fascia cells

Linda Vi1, Anna Njarlangattil1, Yan Wu1, Bing Siang Gan1234 and David B O'Gorman125*

Author Affiliations

1 Cell and Molecular Biology Laboratory, Hand and Upper Limb Centre, Lawson Health Research Institute, London, Canada

2 Department of Surgery, University of Western Ontario, London, Canada

3 Department of Physiology and Pharmacology, University of Western Ontario, London, Canada

4 Department of Medical Biophysics, University of Western Ontario, London, Canada

5 Department of Biochemistry, University of Western Ontario, London, Canada

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BMC Musculoskeletal Disorders 2009, 10:72  doi:10.1186/1471-2474-10-72

Published: 19 June 2009



Dupuytren's Disease (DD) is a debilitating contractile fibrosis of the palmar fascia characterised by excess collagen deposition, contractile myofibroblast development, increased Transforming Growth Factor-β levels and β-catenin accumulation. The aim of this study was to determine if a collagen-enriched environment, similar to in vivo conditions, altered β-catenin accumulation by primary DD cells in the presence or absence of Transforming Growth Factor-β.


Primary DD and patient matched, phenotypically normal palmar fascia (PF) cells were cultured in the presence or absence of type-1 collagen and Transforming Growth Factor-β1. β-catenin and α-smooth muscle actin levels were assessed by western immunoblotting and immunofluorescence microscopy.


DD cells display a rapid depletion of cellular β-catenin not evident in patient-matched PF cells. This effect was not evident in either cell type when cultured in the absence of type-1 collagen. Exogenous addition of Transforming Growth Factor-β1 to DD cells in collagen culture negates the loss of β-catenin accumulation. Transforming Growth Factor-β1-induced α-smooth muscle actin, a marker of myofibroblast differentiation, is attenuated by the inclusion of type-1 collagen in cultures of DD and PF cells.


Our findings implicate type-1 collagen as a previously unrecognized regulator of β-catenin accumulation and a modifier of TGF-β1 signaling specifically in primary DD cells. These data have implications for current treatment modalities as well as the design of in vitro models for research into the molecular mechanisms of DD.