ArticlePloS one2017
Antioxidants and NOX1/NOX4 inhibition blocks TGFβ1-induced CCN2 and α-SMA expression in dermal and gingival fibroblasts.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Review
- Therapeutic Approaches to Systemic Sclerosis: Recent Approvals and Future Candidate Therapies.Clinical reviews in allergy & immunology · 2023Review
- A predicted structure of NADPH Oxidase 1 identifies key components of ROS generation and strategies for inhibition.PloS one · 2023Article
- TET2 Promotes Keloid Hyperplasia by Regulating 5hmC Modification in the TGFβ Promoter Region.Clinical, cosmetic and investigational dermatology · 2023Article
- Inhibitory Effects of 3',4'-Dihydroxyflavonol in a Mouse Model of Glaucoma Filtration Surgery and TGFβ1-Induced Responses in Human Tenon's Fibroblasts.Translational vision science & technology · 2022Article
- Oxidative stress promotes fibrosis in systemic sclerosis through stabilization of a kinase-phosphatase complex.JCI insight · 2022Article
- Molecular Pathogenesis and the Possible Role of Mitochondrial Heteroplasmy in Thoracic Aortic Aneurysm.Life (Basel, Switzerland) · 2021Review
- New promising drugs for the treatment of systemic sclerosis: pathogenic considerations, enhanced classifications, and personalized medicine.Expert opinion on investigational drugs · 2021Review
- Verteporfin inhibits the persistent fibrotic phenotype of lesional scleroderma dermal fibroblasts.Journal of cell communication and signaling · 2021Article
- In vitro biocompatibility of biohybrid polymers membrane evaluated in human gingival fibroblasts.Journal of biomedical materials research. Part B, Applied biomaterials · 2020Article
- Transient Receptor Potential Vanilloid channel regulates fibroblast differentiation and airway remodeling by modulating redox signals through NADPH Oxidase 4.Scientific reports · 2020Article
- Conjunction junction, what's the function? CCN proteins as targets in fibrosis and cancers.American journal of physiology. Cell physiology · 2020Review
- CCN1 expression by fibroblasts is required for bleomycin-induced skin fibrosis.Matrix biology plus · 2019Article
- Comparative RNA sequencing reveals that HPV16 E6 abrogates the effect of E6*I on ROS metabolism.Scientific reports · 2019Article
- Abrogation of transforming growth factor-β-induced tissue fibrosis in mice with a global genetic deletion of Nox4.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Article
- A Potential Link Between Oxidative Stress and Endothelial-to-Mesenchymal Transition in Systemic Sclerosis.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TGFbeta induces fibrogenic responses in fibroblasts. Reactive oxygen species (ROS)/nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) may contribute to fibrogenic responses. Here, we examine if the antioxidant N-acetylcysteine (NAC), the NOX inhibitor diphenyleneiodonium (DPI) and the selective NOX1/NOX4 inhibitor GKT-137831 impairs the ability of TGFbeta to induce profibrotic gene expression in human gingival (HGF) and dermal (HDF) fibroblasts. We also assess if GKT-137831 can block the persistent fibrotic phenotype of lesional scleroderma (SSc) fibroblasts. We use real-time polymerase chain reaction and Western blot analysis to evaluate whether NAC and DPI impair the ability of TGFbeta1 to induce expression of fibrogenic genes in fibroblasts. The effects of GKT-137831 on TGFbeta-induced protein expression and the persistent fibrotic phenotype of lesional scleroderma (SSc) fibroblasts were tested using Western blot and collagen gel contraction analyses. In HDF and HGF, TGFbeta1 induces CCN2, CCN1, endothelin-1 and alpha-smooth muscle actin (SMA) in a fashion sensitive to NAC. Induction of COL1A1 mRNA was unaffected. Similar results were seen with DPI. NAC and DPI impaired the ability of TGFbeta1 to induce protein expression of CCN2 and alpha-SMA in HDF and HGF. GKT-137831 impaired TGFbeta-induced CCN2 and alpha-SMA protein expression in HGF and HDF. In lesional SSc dermal fibroblasts, GKT-137831 reduced alpha-SMA and CCN2 protein overexpression and collagen gel contraction. These results are consistent with the hypothesis that antioxidants or NOX1/4 inhibition may be useful in blocking profibrotic effects of TGFbeta on dermal and gingival fibroblasts and warrant consideration for further development as potential antifibrotic agents.
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