ArticleArthritis and rheumatism2010
Blocking ERK-1/2 reduces tumor necrosis factor alpha-induced interleukin-18 bioactivity in rheumatoid arthritis synovial fibroblasts by induction of interleukin-18 binding protein A.
Article in Arthritis and rheumatism, 2010. 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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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
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- The role of interleukin-18 and interleukin-18 binding protein in K/BxN serum transfer-induced arthritis.Frontiers in immunology · 2023Article
- MiR-129-5p regulates cell proliferation and apoptosis via IGF-1R/Src/ERK/Egr-1 pathway in RA-fibroblast-like synoviocytes.Bioscience reports · 2019Article
- Inflammatory properties of inhibitor of DNA binding 1 secreted by synovial fibroblasts in rheumatoid arthritis.Arthritis research & therapy · 2016Article
- Pharmacological Inactivation of Src Family Kinases Inhibits LPS-Induced TNF-α Production in PBMC of Patients with Behçet's Disease.Mediators of inflammation · 2016Article
- The pathogenic role of angiogenesis in rheumatoid arthritis.Angiogenesis · 2015Review
- Blocking the janus-activated kinase pathway reduces tumor necrosis factor alpha-induced interleukin-18 bioactivity by caspase-1 inhibition.Arthritis research & therapy · 2014Article
- Inhibitor of DNA binding 1 as a secreted angiogenic transcription factor in rheumatoid arthritis.Arthritis research & therapy · 2014Article
- β2 adrenergic activation induces the expression of IL-18 binding protein, a potent inhibitor of isoproterenol induced cardiomyocyte hypertrophy in vitro and myocardial hypertrophy in vivo.Journal of molecular and cellular cardiology · 2012Article
- Blocking of interferon regulatory factor 1 reduces tumor necrosis factor α-induced interleukin-18 bioactivity in rheumatoid arthritis synovial fibroblasts by induction of interleukin-18 binding protein a: role of the nuclear interferon regulatory factor 1-NF-κB-c-jun complex.Arthritis and rheumatism · 2011Article
- Interleukin-18 as an in vivo mediator of monocyte recruitment in rodent models of rheumatoid arthritis.Arthritis research & therapy · 2010Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo examine the mechanism of regulation of interleukin-18 (IL-18) bioactivity by IL-18 binding protein (IL-18BP) induction.
methodsLevels of IL-18 and IL-18BPa in synovial fluid samples from patients with osteoarthritis (OA) or rheumatoid arthritis (RA) were determined by enzyme-linked immunosorbent assays (ELISAs), followed by calculation of free IL-18. IL-18 and IL-18BPa synthesis in RA synovial fibroblasts that had been treated with proinflammatory and antiinflammatory cytokines were assessed by quantitative real-time polymerase chain reaction and ELISA, respectively, followed by IL-18 bioactivity determination using KG-1 cells. Chemical signaling inhibitors were used for determination of the signal transduction pathways involved in IL-18BPa/IL-18 regulation. Tumor necrosis factor alpha (TNFalpha)-induced caspase 1 activity was determined by a colorimetric assay.
resultsIL-18BPa was lower in RA synovial fluid than in OA synovial fluid (P < 0.05; n = 8), and free IL-18 was higher in RA synovial fluid than in OA synovial fluid. TNFalpha induced RA synovial fibroblast IL-18BPa and IL-18 in a time-dependent manner (P < 0.05). Evaluation of signaling pathways suggested that TNFalpha induced IL-18 production through the ERK-1/2, protein kinase Cdelta (PKCdelta), and Src pathways, whereas IL-18BPa synthesis was mediated through the NFkappaB, PKC, Src, and JNK pathways. Furthermore, addition of exogenous IL-18BPa-Fc reduced the RA synovial fibroblast phosphorylation of ERK-1/2 induced by TNFalpha.
conclusionThese results suggest that IL-18BPa reduces IL-18 bioactivity induced by TNFalpha, by regulating the ERK-1/2 pathway in RA synovial fibroblasts. Targeting IL-18 bioactivity by induction or addition of IL-18BPa may provide another therapeutic option in the management of RA.
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