ArticlePharmaceuticals (Basel, Switzerland)2022
Tofacitinib May Inhibit Myofibroblast Differentiation from Rheumatoid-Fibroblast-like Synoviocytes Induced by TGF-β and IL-6.
Article in Pharmaceuticals (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 19 citations in OpenAlex.
- Effectiveness and safety of Janus Kinase inhibitors in patients with rheumatoid arthritis, results from a multicenter observational "real-life" GIRRCS (Gruppo Italiano di Ricerca in Reumatologia Clinica e Sperimentale) study.Clinical rheumatology · 2026Article
- Fibroblast-like Synoviocytes as Therapeutic Targets in Rheumatoid Arthritis: Current Evidence on DMARD-Mediated Modulation.Biomedicines · 2026Review
- Hyperlipidemia exacerbates frozen shoulder fibrosis by activating the TGF-β/Smad2/3 signaling pathway via the TBX5-TNC-Itgα2 axis.iScience · 2026Article
- Integrated multi-platform metabolomics reveals fatty acid-mediated inflammatory signatures in pretibial myxedema.Frontiers in endocrinology · 2026Article
- Article
- Fluorescent probes in autoimmune disease research: current status and future prospects.Journal of translational medicine · 2025Review
- Clinical updates of JAK inhibitors in cutaneous granulomatous diseases.Frontiers in immunology · 2025Review
- JAK Inhibitors in Rheumatoid Arthritis: Immunomodulatory Properties and Clinical Efficacy.International journal of molecular sciences · 2024Review
- The effects of suppressing inflammation by tofacitinib may simultaneously improve glycaemic parameters and inflammatory markers in rheumatoid arthritis patients with comorbid type 2 diabetes: a proof-of-concept, open, prospective, clinical study.Arthritis research & therapy · 2024Article
- Fibrotic pathways and fibroblast-like synoviocyte phenotypes in osteoarthritis.Frontiers in immunology · 2024Review
- Special Issue "Rheumatic Diseases: Pathophysiology, Targeted Therapy, Focus on Vascular and Pulmonary Manifestations 2022".Pharmaceuticals (Basel, Switzerland) · 2023Article
- Advances of the small molecule drugs regulating fibroblast-like synovial proliferation for rheumatoid arthritis.Frontiers in pharmacology · 2023Review
- Role of mitochondria-bound HK2 in rheumatoid arthritis fibroblast-like synoviocytes.Frontiers in immunology · 2023Article
- AXL Inhibits Proinflammatory Factors to Relieve Rheumatoid Arthritis Pain by Regulating the TLR4/NF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
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Authors and funding
14 authors at 4 institutions in 1 country.
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Abstract
During rheumatoid arthritis (RA), the pathogenic role of resident cells within the synovial membrane is suggested, especially for a population frequently referred to as fibroblast-like synoviocytes (FLSs). In this study, we assess the markers of myofibroblast differentiation of RA-FLSs by ex vivo observations and in vitro evaluations following the stimulation with both TGF-β and IL-6. Furthermore, we investigated the possible inhibiting role of tofacitinib, a JAK inhibitor, in this context. Myofibroblast differentiation markers were evaluated on RA synovial tissues by immune-fluorescence or immune-histochemistry. RA-FLSs, stimulated with transforming growth factor (TGF-β) and interleukin-6 (IL-6) with/without tofacitinib, were assessed for myofibroblast differentiation markers expression by qRT-PCR and Western blot. The same markers were evaluated following JAK-1 silencing by siRNA assay. The presence of myofibroblast differentiation markers in RA synovial tissue was significantly higher than healthy controls. Ex vivo, α-SMA was increased, whereas E-Cadherin decreased. In vitro, TGF-β and IL-6 stimulation of RA-FLSs promoted a significant increased mRNA expression of collagen I and α-SMA, whereas E-Cadherin mRNA expression was decreased. In the same conditions, the stimulation with tofacitinib significantly reduced the mRNA expression of collagen I and α-SMA, even if the Western blot did not confirm this finding. JAK-1 gene silencing did not fully prevent the effects of stimulation with TGF-β and IL-6 on these features. TGF-β and IL-6 stimulation may play a role in mediating myofibroblast differentiation from RA-FLSs, promoting collagen I and α-SMA while decreasing E-Cadherin. Following the same stimulation, tofacitinib reduced the increases of both collagen I and α-SMA on RA-FLSs, although further studies are needed to fully evaluate this issue and confirm our results.
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