ArticleMolecular and cellular biochemistry2019
Transforming growth factor β1 promotes fibroblast-like synoviocytes migration and invasion via TGF-β1/Smad signaling in rheumatoid arthritis.
Article in Molecular and cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Comprehensive systematic review and meta-analysis of the TGF-β1 T869C gene polymorphism and autoimmune disease susceptibility.Frontiers in genetics · 2025Pooled it
- Review
- Fibrosis in Immune-Mediated and Autoimmune Disorders.Journal of clinical medicine · 2025Review
- Eurycomanone Blocks TGF-β1-Induced Epithelial-to-Mesenchymal Transition, Migration, and Invasion Pathways in Human Non-Small Cell Lung Cancer Cells by Targeting Smad and Non-Smad Signaling.International journal of molecular sciences · 2025Article
- At Early Rheumatoid Arthritis Stage, the Infectious Spectrum Is Driven by Non-Familial Factors and Anti-CCP Immunization.Journal of clinical medicine · 2024Article
- Identification of the potential regulatory interactions in rheumatoid arthritis through a comprehensive analysis of lncRNA-related ceRNA networks.BMC musculoskeletal disorders · 2023Article
- Involvement of Epithelial-Mesenchymal Transition (EMT) in Autoimmune Diseases.International journal of molecular sciences · 2023Review
- Towards a Unified Approach in Autoimmune Fibrotic Signalling Pathways.International journal of molecular sciences · 2023Review
- Circ_0004712 Silencing Suppresses the Aggressive Changes of Rheumatoid Arthritis Fibroblast-Like Synoviocytes by Targeting miR-633/TRAF6 Axis.Biochemical genetics · 2023Article
- Receptor tyrosine kinase C-kit promotes a destructive phenotype of FLS in osteoarthritis via intracellular EMT signaling.Molecular medicine (Cambridge, Mass.) · 2023Article
- Article
- Global trends in research of fibroblasts associated with rheumatoid diseases in the 21st century: A bibliometric analysis.Frontiers in immunology · 2023Article
- TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases.Mediterranean journal of rheumatology · 2022Review
- Tofacitinib May Inhibit Myofibroblast Differentiation from Rheumatoid-Fibroblast-like Synoviocytes Induced by TGF-β and IL-6.Pharmaceuticals (Basel, Switzerland) · 2022Article
- miR-135a-5p mediated down-regulation of STAT6 inhibits proliferation and induces apoptosis of fibroblast-like synoviocytes in rheumatoid arthritis.American journal of translational research · 2022Article
- Platelet signaling at the nexus of innate immunity and rheumatoid arthritis.Frontiers in immunology · 2022Review
- Association analysis of juvenile idiopathic arthritis genetic susceptibility factors in Estonian patients.Clinical rheumatology · 2021Article
- Losartan protects against osteoarthritis by repressing the TGF-β1 signaling pathwayJournal of orthopaedic translation · 2021Article
- Signalling and putative therapeutic molecules on the regulation of synoviocyte signalling in rheumatoid arthritis.Bone & joint research · 2021Article
- Advanced oxidation protein products induce inflammatory responses and invasive behaviour in fibroblast-like synoviocytes via the RAGE-NF-κB pathway.Bone & joint research · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Migration and invasion are important characteristics of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs), which are involved in joint damage and contribute to rheumatoid arthritis (RA) pathology. However, the underlying mechanisms remain unclear. Because epithelial-mesenchymal transition (EMT) is a key mechanism related to migration and invasion in cancer cells, we investigated the relationship between EMT and RA-FLSs and explored whether the transforming growth factor β1 (TGF-β1)/Smad signaling pathway is involved. In vivo, fibroblast-like synoviocytes (FLSs) were isolated from the synovium of RA or osteoarthritis (OA) patients and cultured for 4-8 passages. EMT markers were detected by immunofluorescence and Western blotting. RA-FLSs were treated with TGF-β1 or Smad2/3 small interfering RNA (siRNA), EMT markers were detected, and migration and invasion were assessed by Transwell assays. EMT markers could be detected in FLSs; when compared with osteoarthritis fibroblast-like synoviocytes (OA-FLSs), E-cadherin and vimentin decreased, while N-cadherin and α-smooth muscle actin (α-SMA) increased in RA-FLSs. Furthermore, TGF-β1 enhanced migration and invasion by inducing EMT via activating Smad2/3 in RA-FLSs. Phosphorylation of Smad2/3 was accompanied by degradation of Smad3. Silencing Smad2/3 blocked EMT and inhibited the migration and invasion induced by TGF-β1. Matrix metalloproteinase 9 (MMP9) and vimentin were not affected when cells were treated with TGF-β1 or Smad2/3 siRNA. The TGF-β1/Smad signaling pathway is involved in EMT and contributes to migration and invasion in RA-FLSs. Interestingly, vimentin decreased in RA-FLSs, but there is no correlation between vimentin and TGF-β1/Smad signaling pathway. Thus, further research on vimentin should be conducted.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.