<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>4(1)</volume><submitter>Onnheim K</submitter><pubmed_abstract>&lt;h4>Objective&lt;/h4> To investigate whether articular chondrocytes from rheumatoid arthritis (RA) patients have acquired a proinflammatory phenotype. &lt;h4>Method&lt;/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. &lt;h4>Results&lt;/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. &lt;h4>Conclusions&lt;/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.</pubmed_abstract><journal>Osteoarthritis and cartilage open</journal><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9718183</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Rheumatoid arthritis chondrocytes produce increased levels of pro-inflammatory proteins</pubmed_title><pmcid>PMC9718183</pmcid><pubmed_authors>Huang S</pubmed_authors><pubmed_authors>Strid Holmertz A</pubmed_authors><pubmed_authors>Jonsson C</pubmed_authors><pubmed_authors>Andersson S</pubmed_authors><pubmed_authors>Gjertsson I</pubmed_authors><pubmed_authors>Lonnblom E</pubmed_authors><pubmed_authors>Holmdahl R</pubmed_authors><pubmed_authors>Onnheim K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Rheumatoid arthritis chondrocytes produce increased levels of pro-inflammatory proteins</name><description>&lt;h4>Objective&lt;/h4> To investigate whether articular chondrocytes from rheumatoid arthritis (RA) patients have acquired a proinflammatory phenotype. &lt;h4>Method&lt;/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. &lt;h4>Results&lt;/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. &lt;h4>Conclusions&lt;/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.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jan</publication><modification>2025-04-26T20:48:32.527Z</modification><creation>2025-04-06T16:32:27.955Z</creation></dates><accession>S-EPMC9718183</accession><cross_references/></HashMap>