{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["4(1)"],"submitter":["Onnheim K"],"pubmed_abstract":["<h4>Objective</h4> To investigate whether articular chondrocytes from rheumatoid arthritis (RA) patients have acquired a proinflammatory phenotype. <h4>Method</h4> Articular cartilage explants from RA patients and healthy controls (HC) were cultured with or without interleukin (IL)-1β for two weeks. Protein levels of cytokines and metalloproteinases (MMPs) in the supernatant were measured by LUMINEX, mRNA with qPCR and nitrogen oxide (NO) levels with Griess assay. <h4>Results</h4> Within 24 ​h after culture, cartilage explants from RA spontaneously produced MMP-1 and MMP-13, and matrix components (aggrecan and collagen type IV) were released. In addition, the RA explants released higher levels of tumor necrosis factor, interferon-γ, IL-33, IL-18, vascular endothelial growth factor-A, IL-6 but not IL-8, and granulocyte-macrophage colony-stimulating factor (GM-CSF) as compared with HC. During two weeks of incubation the higher levels did not diminish. IL-1β stimulation further increased the levels of IL-6, IL-8 and GM-CSF, mainly in RA explants, and induced increased levels of NO in the supernatant from both HC and RA explants, as a result of chondrocyte activation. <h4>Conclusions</h4> RA chondrocytes are activated with a proinflammatory profile involving the production of cytokines as well as MMP-1 and MMP-13, that can lead to release of matrix molecules after activation, which suggests that the chondrocytes have a proinflammatory phenotype and thereby an active role in the pathogenesis."],"journal":["Osteoarthritis and cartilage open"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9718183"],"repository":["biostudies-literature"],"pubmed_title":["Rheumatoid arthritis chondrocytes produce increased levels of pro-inflammatory proteins"],"pmcid":["PMC9718183"],"pubmed_authors":["Huang S","Strid Holmertz A","Jonsson C","Andersson S","Gjertsson I","Lonnblom E","Holmdahl R","Onnheim K"],"additional_accession":[]},"is_claimable":false,"name":"Rheumatoid arthritis chondrocytes produce increased levels of pro-inflammatory proteins","description":"<h4>Objective</h4> To investigate whether articular chondrocytes from rheumatoid arthritis (RA) patients have acquired a proinflammatory phenotype. <h4>Method</h4> Articular cartilage explants from RA patients and healthy controls (HC) were cultured with or without interleukin (IL)-1β for two weeks. Protein levels of cytokines and metalloproteinases (MMPs) in the supernatant were measured by LUMINEX, mRNA with qPCR and nitrogen oxide (NO) levels with Griess assay. <h4>Results</h4> Within 24 ​h after culture, cartilage explants from RA spontaneously produced MMP-1 and MMP-13, and matrix components (aggrecan and collagen type IV) were released. In addition, the RA explants released higher levels of tumor necrosis factor, interferon-γ, IL-33, IL-18, vascular endothelial growth factor-A, IL-6 but not IL-8, and granulocyte-macrophage colony-stimulating factor (GM-CSF) as compared with HC. During two weeks of incubation the higher levels did not diminish. IL-1β stimulation further increased the levels of IL-6, IL-8 and GM-CSF, mainly in RA explants, and induced increased levels of NO in the supernatant from both HC and RA explants, as a result of chondrocyte activation. <h4>Conclusions</h4> RA chondrocytes are activated with a proinflammatory profile involving the production of cytokines as well as MMP-1 and MMP-13, that can lead to release of matrix molecules after activation, which suggests that the chondrocytes have a proinflammatory phenotype and thereby an active role in the pathogenesis.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2025-04-26T20:48:32.527Z","creation":"2025-04-06T16:32:27.955Z"},"accession":"S-EPMC9718183","cross_references":{}}