TNF-α Suppresses α-Smooth Muscle Actin Expression in Human Dermal Fibroblasts: An Implication for Abnormal Wound Healing
Open accessAbstract
Abnormal wound healing encompasses a wide spectrum, from chronic wounds to hypertrophic scars. Both conditions are associated with an abnormal cytokine profile in the wound bed. In this study, we sought to understand the dynamic relationships between myofibroblast differentiation and mechanical performance of the collagen matrix under tissue growth factor-beta (TGF-beta) and tumor necrosis factor-alpha (TNF-alpha) stimulation. We found TGF-beta increased alpha-smooth muscle actin (alpha-SMA) and TNF-alpha alone decreased the basal alpha-SMA expression. When TGF-beta1 and TNF-alpha were both added, the alpha-SMA expression was suppressed below the baseline. Real-time PCR showed that TNF-alpha suppresses TGF-beta1-induced myofibroblast (fibroproliferative) phenotypic genes, for example, alpha-SMA, collagen type 1A, and fibronectin at the mRNA level. TNF-alpha suppresses TGF-beta1-induced gene expression by affecting its mRNA stability. Our results further showed that TNF-alpha inhibits TGF-beta1-induced Smad-3 phosphorylation via Jun N-terminal kinase signaling. Mechanical testing showed that TNF-alpha decreases the stiffness and contraction of the lattices after 5 days in culture. We proposed that changes in alpha-SMA, collagen, and fibronectin expression result in decreased contraction and stiffness of collagen matrices. Therefore, the balance of cytokines in a wound defines the mechanical properties of the extracellular matrix and optimal wound healing.
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In dermal fibroblasts, TNFα can inhibit αSMA expression by inhibiting TGFβ signaling.
“However, in dermal fibroblasts TNFα can inhibit αSMA expression by inhibiting TGFβ signaling (124).”
From Unraveling SSc Pathophysiology; The Myofibroblast (2018) · cites this paper as [124]
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- Authors
- Goldberg, M. T., Han, Y.-P., Yan, C., Shaw, M. C., & Garner, W. L.
- Affiliations
- University of Southern California (US)
- California Lutheran University (US)
- Corresponding author
- Garner, Warren L.
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2007-11
- Volume
- 127
- Issue
- 11
- Pages
- 2645-2655
- ISSN
- 0022-202X (ISSN-L)
- PMC
- PMC2366884
- OpenAlex
- W2010619374
- Cited by
- 219
- References
- 42
- Citations by year
- 2026: 10 · 2025: 19 · 2024: 17 · 2023: 6 · 2022: 14 · 2021: 16 · 2020: 12 · 2019: 12 · 2018: 12 · 2017: 14 · 2016: 7 · 2015: 15 · 2014: 13 · 2013: 5 · 2012: 13
- FWCI
- 7.93
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM050967)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR051558)
- Topics
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Dermatology › Dermatologic Treatments and Research
- Keywords
- TNF-α, alpha-smooth muscle actin, TGF-β1, dermal fibroblasts, myofibroblast differentiation, wound healing, hypertrophic scars, chronic wounds, fibronectin, mRNA stability, JNK signaling, extracellular matrix stiffness, collagen matrix contraction, cytokine balance
- MeSH terms
- Actins, Cells, Cultured, Chronic Disease, Fibroblasts, Fibronectins, Humans, RNA, Messenger, Tumor Necrosis Factor-alpha, Wound Healing, Wounds and Injuries, Signal Transduction, Cicatrix, Hypertrophic, Dermis, Mitogen-Activated Protein Kinase Kinases, Collagen Type I, Smad3 Protein, Transforming Growth Factor beta1
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