ArticleCell death & disease2017
Synovial cell death is regulated by TNF-α-induced expression of B-cell activating factor through an ERK-dependent increase in hypoxia-inducible factor-1α.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Hypoxia as an amplifier of synovial inflammation in rheumatoid arthritis.Nature reviews. Rheumatology · 2026Review
- Investigation of Cytokine Profiles, the Expression of Genes Involved in Somatic Hypermutation and Peripheral Tolerance, and Their Correlation with Autoantibody Levels in Northern-Thai Immunodeficient Patients Carrying Anti-Interferon-γ Autoantibodies.International journal of molecular sciences · 2026Article
- Eleutheroside E Attenuates Hypobaric Hypoxia-Induced High Altitude Pulmonary Edema by Regulating Ferritinophagy-Mediated Ferroptosis via Keap1-Nrf2 Regulatory Axis.Journal of inflammation research · 2026Article
- Programmed Cell Death in Rheumatoid Arthritis.Journal of inflammation research · 2025Review
- Adalimumab Effectively Decreases Inflammation Downstream of TNFα Signaling in Synoviocytes from Extended Oligoarticular Juvenile Idiopathic Arthritis.Rheumatology and therapy · 2024Article
- Article
- HeLa Cervical Cancer Cells Are Maintained by Nephronophthisis 3-Associated Primary Cilium Formation via ROS-Induced ERK and HIF-1α Activation under Serum-Deprived Normoxic Condition.International journal of molecular sciences · 2022Article
- Dihydroarteannuin Ameliorates Collagen-Induced ArthritisFrontiers in pharmacology · 2022Article
- B Cell Adhesion to Fibroblast-Like Synoviocytes Is Up-Regulated by Tumor Necrosis Factor-Alpha via Expression of Human Vascular Cell Adhesion Molecule-1 Mediated by B Cell-Activating Factor.International journal of molecular sciences · 2021Article
- CXCR4 promotes B cell viability by the cooperation of nuclear factor (erythroid-derived 2)-like 2 and hypoxia-inducible factor-1α under hypoxic conditions.Cell death & disease · 2021Article
- Metabolic Reprogramming and Inflammatory Response Induced by D-Lactate in Bovine Fibroblast-Like Synoviocytes Depends on HIF-1 Activity.Frontiers in veterinary science · 2021Article
- Therapeutic Targeting of Transcription Factors to Control the Cytokine Release Syndrome in COVID-19.Frontiers in pharmacology · 2021Article
- Apoptosis, Autophagy, NETosis, Necroptosis, and Pyroptosis Mediated Programmed Cell Death as Targets for Innovative Therapy in Rheumatoid Arthritis.Frontiers in immunology · 2021Review
- Article
- Synovial Cell Migration is Associated with B Cell Activating Factor Expression Increased by TNFα or Decreased by KR33426.Biomolecules & therapeutics · 2020Article
- Anti-inflammatory effects of Jingshu Keli capsule and its components on human synoviocyte MH7A cells.Arthroplasty (London, England) · 2020Article
- Parallel comparison of fibroblast-like synoviocytes from the surgically removed hyperplastic synovial tissues of rheumatoid arthritis and osteoarthritis patients.BMC musculoskeletal disorders · 2019Article
- Article
- Chlorogenic Acid Inhibits BAFF Expression in Collagen-Induced Arthritis and Human Synoviocyte MH7A Cells by Modulating the Activation of the NF-Journal of immunology research · 2019Article
- [2-deoxyglucose inhibits angiogenesis of rheumatoid arthritis via activating AMPK pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B-cell activating factor (BAFF) has a role in the maturation and maintenance of B cells and is associated with rheumatoid arthritis (RA). Here, we investigated whether tumor necrosis factor (TNF)-α-induced BAFF expression controls the survival of fibroblast-like synoviocytes (FLS) and whether their survival can be regulated by TNF-α-mediated upregulation of hypoxia-inducible factor (HIF)-1α using MH7A synovial cells transfected with the SV40 T antigen. More TNF-α-treated cells died compared with the control. Survival was increased by incubation with Z-VAD but inhibited after transfection with BAFF-siRNA. Both BAFF and HIF-1α expression were enhanced when MH7A cells were treated with TNF-α. TNF-α-induced BAFF expression decreased in response to HIF-1α-siRNA, whereas it increased under hypoxia or by overexpressing HIF-1α. The HIF-1α binding site on the BAFF promoter (-693 to -688 bp) was confirmed by chromatin immunoprecipitation assay to detect the -750 to -501 bp and -800 to -601 bp regions. The BAFF promoter increased in response to TNF-α treatment or overexpression of HIF-1α. However, TNF-α-induced BAFF expression and promoter activity decreased after treatment with the ERK inhibitor PD98059. Cell death was enhanced by PD98059 but was inhibited by overexpression of HIF-1α. Taken together, our results demonstrate that BAFF expression to control synovial cell survival was regulated by HIF-1α binding to the BAFF promoter, and suggest for the first time that HIF-1α might be involved in the production of inflammatory cytokines to regulate the physiological function of rheumatic FLS.
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