ArticleScientific reports2020
Dermal fibroblasts have different extracellular matrix profiles induced by TGF-β, PDGF and IL-6 in a model for skin fibrosis.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
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Who cites it
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
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- Skin Anti-Aging Efficacy of Enzyme-Treated Supercritical Caviar Extract: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial.Nutrients · 2023Trial
- Enterovirus 71 drives TLR2-NF-κB-dependent inflammatory skeletal muscle injury in neonatal BALB/c mice.Microbiology spectrum · 2026Article
- Targeting fibroblast activation suppresses chemotherapy-induced pro-invasive remodeling of the extracellular matrix.bioRxiv : the preprint server for biology · 2026Article
- A Layered Framework for Biological Aesthetics: A Narrative Review of Regenerative Medicine in Cosmetic Science.Cureus · 2026Review
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- Mathematical Modeling of Systemic Sclerosis and Its Treatment.Bulletin of mathematical biology · 2026Article
- Ancestry-linked IL-10 signaling and macrophage activation modulate fibroblast responses to oxidative stress in a PEG-based microphysiological system.npj biomedical innovations · 2026Article
- Collagen-derived biomarkers reveal distinct fibrotic responses among cancer-associated fibroblasts.Scientific reports · 2026Article
- Probenecid-Mediated Pannexin-1 Inhibition Preserves βFGF-Driven Regenerative Responses in Human Dermal Fibroblasts.International journal of molecular sciences · 2026Article
- Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling.Cell reports. Medicine · 2026Article
- Article
- CD109 Deletion Promotes Myofibroblast Differentiation and Smad-Dependent Matrix Accumulation in Skin Fibrosis.International journal of molecular sciences · 2026Article
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- Modeling CAF-tumor interactions to overcome therapy resistance.Journal of experimental & clinical cancer research : CR · 2026Review
- MMPs at Work: Deciphering Their Role in the Cellular Mechanisms of Orthodontic Tooth Movement.International journal of molecular sciences · 2026Review
- MDI1228, a topical pan-JAK inhibitor, disrupts dermal fibroblast-T cell chemokine crosstalk to resolve allergic contact and atopic dermatitis.Frontiers in immunology · 2026Article
- FGF/FGFR signaling at the immune-stromal interface in autoimmune rheumatic diseases: from tissue remodeling to translational opportunities.Frontiers in immunology · 2026Review
- Enhanced Facial Rejuvenation: Biostimulatory Effects of Hylan Gel Dermal Filler DX on Collagen Synthesis and Tissue Regeneration.Aesthetic plastic surgery · 2026Article
- Cellular and molecular changes in the skin driving increased nociception and pain during burn injury and repair.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
31 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Different stimulants might induce different extracellular matrix profiles. It is essential to gain an understanding and quantification of these changes to allow for focused anti-fibrotic drug development. This study investigated the expression of extracellular matrix by dermal fibroblast mimicking fibrotic skin diseases as SSc using clinically validated biomarkers. Primary healthy human dermal fibroblasts were grown in media containing FICOLL. The cells were stimulated with PDGF-AB, TGF-β1, or IL-6. Anti-fibrotic compounds (iALK-5, Nintedanib) were added together with growth factors. Biomarkers of collagen formation and degradation together with fibronectin were evaluated by ELISAs in the collected supernatant. Immunohistochemical staining was performed to visualize fibroblasts and proteins, while selected gene expression levels were examined through qPCR. TGF-β and PDGF, and to a lesser extent IL-6, increased the metabolic activity of the fibroblasts. TGF-β primarily increased type I collagen and fibronectin protein and gene expression together with αSMA. PDGF stimulation resulted in increased type III and VI collagen formation and gene expression. IL-6 decreased fibronectin levels. iALK5 could inhibit TGF-β induced fibrosis while nintedanib could halt fibrosis induced by TGF-β or PDGF. Tocilizumab could not inhibit fibrosis induced in this model. The extent and nature of fibrosis are dependent on the stimulant. The model has potential as a pre-clinical model as the fibroblasts fibrotic phenotype could be reversed by an ALK5 inhibitor and Nintedanib.
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