ArticleFrontiers in molecular biosciences2015
Inflammatory Gene Expression Upon TGF-β1-Induced p38 Activation in Primary Dupuytren's Disease Fibroblasts.
Article in Frontiers in molecular biosciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Evaluation of Nile Tilapia (ACS biomaterials science & engineering · 2026Pooled it
- CD206Circulation · 2025Article
- TEAD4-mediated upregulation of LPAR3 augments hepatic stellate cell activation in portal hypertension.Cell biology and toxicology · 2025Article
- New genetic prognostic biomarkers in primary central nervous system lymphoma (PCNSL).Brain and behavior · 2021Article
- The Role of IL-6 in Skin Fibrosis and Cutaneous Wound Healing.Biomedicines · 2020Review
- Update on the role of molecular factors and fibroblasts in the pathogenesis of Dupuytren's disease.Journal of cell communication and signaling · 2016Article
- Connective Tissue Degeneration: Mechanisms of Palmar Fascia Degeneration (Dupuytren's Disease).Current molecular biology reportsReview
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesInflammation is an underlying mechanism behind fibrotic processes and differentiation of cells into myofibroblasts. Presented study therefore provides new data on activation of autoimmune and inflammatory immune response genes that accompany activation of p38 and cell differentiation in primary cells derived from Dupuytren's disease (DD) patients.
methodsPrimary non-Dupuytren's disease cells (ND) were isolated from macroscopically unaffected palmar fascia adjacent to diseased tissue obtained from patients diagnosed with the last stage of DD and cultured in vitro. Gene expression, collagen gel contraction assay and analysis of secreted proteins were performed in ND cells treated with TGF-β1 and/or inhibitor of p38 phosphorylation.
resultsDuring differentiation of ND fibroblasts, increased expression of immune response genes PAI-1, TIMP-1, CCL11, and IL-6 was found. These changes were accompanied by increased cell contractility and activation of p38 and its target kinase MK2. Inhibition of p38 phosphorylation reversed these processes in vitro.
conclusionsTGF-β1 induced p38 phosphorylation in ND cells grown from macroscopically unaffected palmar fascia adjacent to diseased tissue from DD patients. This was accompanied by activation of the cytokine genes CCL-11 and IL-6 and secretion of extracellular matrix regulatory proteins PAI-1 and TIMP-1. A combined approach directed toward inflammation and p38 MAPK-mediated processes in DD might be considered for improving management of DD patients and prevention of recurrence.
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