FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2808707777> ?p ?o ?g. }

• W2808707777 abstract "Background Synovitis in inflammatory osteoarthritis (OA) is driven by locally released DAMPs like S100A8/A9 proteins that have been shown to enhance joint destruction. S100A8/A9 induce ROS (reactive oxygen species) release by phagocytes in OA synovium via the NADPH-oxidase 2 (NOX2)-complex. Assembly of this complex is dependent on the neutrophils cytosolic factor (Ncf1). In this complex, the NOX2 protein is responsible for ROS production. Objectives In the present study we investigated whether NOX2-derived ROS are involved in joint pathology during collagenase-induced OA (CiOA). Methods CiOA was induced in knee joints of wild type (WT) and Ncf1-deficient (Ncf1 */* ) mice. Synovial gene expression of NOX2-subunits was measured with qRT-PCR. Joint pathology was assessed using histology and antibodies against aggrecan neo-epitope VDIPEN. Levels of inflammatory proteins were measured with Luminex or ELISA. Phagocytes present in synovium, blood, bone marrow and spleen were analysed with flow cytometry. Extracellular ROS production by bone marrow-derived phagocytes was measured using an Amplex Red ROS detection assay. Results CiOA induction in knee joints of WT mice caused significantly increased synovial gene expression of NOX2 subunits. On day 7 of CiOA, synovial thickening, synovial S100A8/A9 levels and synovial percentages of inflammatory macrophages, PMNs, and monocytes were comparable between WT and Ncf1 */* mice. Cartilage damage and MMP activity, as measured by VDIPEN staining, were comparable, as well as levels of inflammatory mediators in serum and phagocyte percentages in blood, bone marrow and spleen. On day 42 of CiOA, synovitis, cartilage damage, and osteophyte formation in Ncf1 */* mice were unaltered when compared to WT mice. ROS production by Ncf1 */* PMNs was completely absent but Ncf1 */* macrophages, the more predominant phagocyte involved in development of pathology during CiOA, produced ROS in similar amounts as WT macrophages. Ncf1 deficiency thus seems to exclusively affect PMNs, this surprising finding might explain the lack of differences observed between CiOA development in WT and Ncf1 */* mice. ROS production by WT and Ncf1 */* macrophages was strongly upregulated by S100A8 and almost completely inhibited by the pan-NOX inhibitor diphenyleneiodonium chloride (DPI). In order to determine whether NOX1 complexes caused the compensation responsible for Ncf1 independent ROS production, we co-stimulated Ncf1 */* macrophages with NOX1-specific inhibitor ML171. However, no ML171-induced inhibition of ROS production was observed. Conclusions Absence of PMN-derived ROS does not alter synovitis and joint pathology in S100A8/A9-driven experimental inflammatory OA. The mechanism that enables Ncf1-independent ROS production by macrophages should be further investigated. Disclosure of Interest None declared" @default.
• W2808707777 created "2018-06-21" @default.
• W2808707777 creator A5033385807 @default.
• W2808707777 creator A5033535335 @default.
• W2808707777 creator A5058446721 @default.
• W2808707777 creator A5072990340 @default.
• W2808707777 creator A5074534756 @default.
• W2808707777 date "2018-06-01" @default.
• W2808707777 modified "2023-09-26" @default.
• W2808707777 title "SAT0067 Role of nox2-derived reactive oxygen species in s100a8/a9-driven inflammatory osteoarthritis" @default.
• W2808707777 doi "https://doi.org/10.1136/annrheumdis-2018-eular.5421" @default.
• W2808707777 hasPublicationYear "2018" @default.
• W2808707777 type Work @default.
• W2808707777 sameAs 2808707777 @default.
• W2808707777 citedByCount "0" @default.
• W2808707777 crossrefType "proceedings-article" @default.
• W2808707777 hasAuthorship W2808707777A5033385807 @default.
• W2808707777 hasAuthorship W2808707777A5033535335 @default.
• W2808707777 hasAuthorship W2808707777A5058446721 @default.
• W2808707777 hasAuthorship W2808707777A5072990340 @default.
• W2808707777 hasAuthorship W2808707777A5074534756 @default.
• W2808707777 hasBestOaLocation W28087077771 @default.
• W2808707777 hasConcept C105702510 @default.
• W2808707777 hasConcept C142724271 @default.
• W2808707777 hasConcept C153911025 @default.
• W2808707777 hasConcept C160448771 @default.
• W2808707777 hasConcept C197534660 @default.
• W2808707777 hasConcept C203014093 @default.
• W2808707777 hasConcept C204787440 @default.
• W2808707777 hasConcept C2776164576 @default.
• W2808707777 hasConcept C2776268809 @default.
• W2808707777 hasConcept C2776914184 @default.
• W2808707777 hasConcept C2777077863 @default.
• W2808707777 hasConcept C2777700362 @default.
• W2808707777 hasConcept C2778557267 @default.
• W2808707777 hasConcept C2779244835 @default.
• W2808707777 hasConcept C2779719074 @default.
• W2808707777 hasConcept C2780007613 @default.
• W2808707777 hasConcept C2780550940 @default.
• W2808707777 hasConcept C2780931953 @default.
• W2808707777 hasConcept C3020332539 @default.
• W2808707777 hasConcept C48349386 @default.
• W2808707777 hasConcept C71924100 @default.
• W2808707777 hasConcept C86803240 @default.
• W2808707777 hasConcept C95444343 @default.
• W2808707777 hasConceptScore W2808707777C105702510 @default.
• W2808707777 hasConceptScore W2808707777C142724271 @default.
• W2808707777 hasConceptScore W2808707777C153911025 @default.
• W2808707777 hasConceptScore W2808707777C160448771 @default.
• W2808707777 hasConceptScore W2808707777C197534660 @default.
• W2808707777 hasConceptScore W2808707777C203014093 @default.
• W2808707777 hasConceptScore W2808707777C204787440 @default.
• W2808707777 hasConceptScore W2808707777C2776164576 @default.
• W2808707777 hasConceptScore W2808707777C2776268809 @default.
• W2808707777 hasConceptScore W2808707777C2776914184 @default.
• W2808707777 hasConceptScore W2808707777C2777077863 @default.
• W2808707777 hasConceptScore W2808707777C2777700362 @default.
• W2808707777 hasConceptScore W2808707777C2778557267 @default.
• W2808707777 hasConceptScore W2808707777C2779244835 @default.
• W2808707777 hasConceptScore W2808707777C2779719074 @default.
• W2808707777 hasConceptScore W2808707777C2780007613 @default.
• W2808707777 hasConceptScore W2808707777C2780550940 @default.
• W2808707777 hasConceptScore W2808707777C2780931953 @default.
• W2808707777 hasConceptScore W2808707777C3020332539 @default.
• W2808707777 hasConceptScore W2808707777C48349386 @default.
• W2808707777 hasConceptScore W2808707777C71924100 @default.
• W2808707777 hasConceptScore W2808707777C86803240 @default.
• W2808707777 hasConceptScore W2808707777C95444343 @default.
• W2808707777 hasLocation W28087077771 @default.
• W2808707777 hasOpenAccess W2808707777 @default.
• W2808707777 hasPrimaryLocation W28087077771 @default.
• W2808707777 hasRelatedWork W1876872825 @default.
• W2808707777 hasRelatedWork W1956735771 @default.
• W2808707777 hasRelatedWork W1986171947 @default.
• W2808707777 hasRelatedWork W2020460212 @default.
• W2808707777 hasRelatedWork W2047858144 @default.
• W2808707777 hasRelatedWork W2064741117 @default.
• W2808707777 hasRelatedWork W2066350271 @default.
• W2808707777 hasRelatedWork W2074173681 @default.
• W2808707777 hasRelatedWork W2078286379 @default.
• W2808707777 hasRelatedWork W2314559141 @default.
• W2808707777 hasRelatedWork W2334671941 @default.
• W2808707777 hasRelatedWork W2541470031 @default.
• W2808707777 hasRelatedWork W2754547368 @default.
• W2808707777 hasRelatedWork W2770416369 @default.
• W2808707777 hasRelatedWork W2793866905 @default.
• W2808707777 hasRelatedWork W2890181947 @default.
• W2808707777 hasRelatedWork W2899840395 @default.
• W2808707777 hasRelatedWork W2994828781 @default.
• W2808707777 hasRelatedWork W3126690131 @default.
• W2808707777 hasRelatedWork W3179039966 @default.
• W2808707777 isParatext "false" @default.
• W2808707777 isRetracted "false" @default.
• W2808707777 magId "2808707777" @default.
• W2808707777 workType "article" @default.