A Human Skin Model Recapitulates Systemic Sclerosis Dermal Fibrosis and Identifies COL22A1 as a TGFβ Early Response Gene that Mediates Fibroblast to Myofibroblast Transition
Open accessAbstract
Systemic sclerosis (SSc) is a complex multi-system autoimmune disease characterized by immune dysregulation, vasculopathy, and organ fibrosis. Skin fibrosis causes high morbidity and impaired quality of life in affected individuals. Animal models do not fully recapitulate the human disease. Thus, there is a critical need to identify ex vivo models for the dermal fibrosis characteristic of SSc. We identified genes regulated by the pro-fibrotic factor TGFβ in human skin maintained in organ culture. The molecular signature of human skin overlapped with that which was identified in SSc patient biopsies, suggesting that this model recapitulates the dermal fibrosis characteristic of the human disease. We further characterized the regulation and functional impact of a previously unreported gene in the setting of dermal fibrosis, COL22A1, and show that silencing COL22A1 significantly reduced TGFβ-induced ACTA2 expression. COL22A1 expression was significantly increased in dermal fibroblasts from patients with SSc. In summary, we identified the molecular fingerprint of TGFβ in human skin and demonstrated that COL22A1 is associated with the pathogenesis of fibrosis in SSc as an early response gene that may have important implications for fibroblast activation. Further, this model will provide a critical tool with direct relevance to human disease to facilitate the assessment of potential therapies for fibrosis.
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Activation of myofibroblasts is part of physiological wound repair; in chronic injury and inflammatory fibrotic conditions, persistent activation exacerbates disease progression.
“Activation of myofibroblasts is itself part of physiological wound repair following tissue injury, whereas in chronic injury and inflammatory fibrotic conditions their persistent activation exacerbates the disease progression [132,133,134,135].”
From Cellular and Molecular Mechanisms in the Pathogenesis of Classical, Vascular, and Hypermobile Ehlers‒Danlos Syndromes (2019) · cites this paper as [135]
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- Authors
- Watanabe, T., Baker Frost, D., Mlakar, L., Heywood, J., da Silveira, W. A., Hardiman, G., & Feghali-Bostwick, C.
- Affiliations
- Medical University of South Carolina (US)
- Division of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, 96 Jonathan Lucas St, MSC 637, Charleston, SC 29425, USA
- Center for Genomic Medicine, Bioinformatics, Medical University of South Carolina, Charleston, SC 29425, USA
- Queen's University Belfast (GB)
- Venue
- Genes
- Publisher
- MDPI AG
- Published
- 2019-01-22
- Volume
- 10
- Issue
- 2
- Pages
- 75
- ISSN
- 2073-4425 (ISSN-L)
- PMC
- PMC6409682
- OpenAlex
- W2914181334
- Cited by
- 33
- References
- 36
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 5 · 2023: 1 · 2022: 10 · 2021: 5 · 2020: 1 · 2019: 2
- FWCI
- 3.31
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- Genes (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research Portal (Queen's University Belfast) (acceptedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (K24AR060297, KL2TR001452, UL1TR001450)
- E. Carwile LeRoy, MD, Endowed Research Fellowship (N/A)
- SmartState and Kitty Trask Holt Endowment (N/A)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Systemic Sclerosis and Related Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Rheumatology › Dupuytren's Contracture and Treatments
- Keywords
- systemic sclerosis, skin fibrosis, COL22A1, TGF-beta, myofibroblast differentiation, ACTA2, dermal fibroblasts, fibrosis pathogenesis, early response genes
- MeSH terms
- Actins, Cells, Cultured, Collagen, Fibrosis, Humans, Scleroderma, Systemic, Skin, Transforming Growth Factor beta, Myofibroblasts
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