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Elevated transforming growth factor β and mitogen-activated protein kinase pathways mediate fibrotic traits of Dupuytren's disease fibroblasts by Carola Krause; Peter Kloen; Peter ten Dijke is a Medicine article available to read on EtoBox.

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## Background Dupuytren's disease is a fibroproliferative disorder of the palmar fascia. The treatment used to date has mostly been surgery, but there is a high recurrence rate. Transforming growth factor β (TGF-β) has been implicated as a key stimulator of myofibroblast activity and fascial contraction in Dupuytren's disease. ## Results We studied Dupuytren's fibroblasts in tissues __ex vivo__ and in cells cultured __in vitro__ and found increased TGF-β expression compared to control fibroblasts. This correlated not only with elevated expression and activation of downstream Smad effectors but also with overactive extracellular signal-regulated kinase 1/2 (ERK1/2)/mitogen-activated protein (MAP) kinase signalling. Treatment with the TGF-β type I receptor kinase inhibitor SB-431542 and bone morphogenetic protein 6 (BMP6) led to inhibition of elevated Smad and ERK1/2/MAP kinase signalling as well as to inhibition of the increased contractility of Dupuytren's fibroblasts. BMP6 attenuated TGF-β expression in Dupuytren's fibroblasts, but not in control fibroblasts. Platelet-derived growth factor (PDGF) expression was strongly promoted by TGF-β in Dupuytren's fibroblasts and was curbed b

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Author

Carola Krause; Peter Kloen; Peter ten Dijke

Publisher

BioMed Central; Springer (Biomed Central Ltd.); [London]: BioMed Central, 2008-; Springer Science and Business Media LLC (ISSN 1755-1536)

Published

2011

Language

EN

Field

Medicine (Health Sciences)