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dc.contributor.authorNorling, LVen_US
dc.contributor.authorHeadland, SEen_US
dc.contributor.authorDalli, Jen_US
dc.contributor.authorArnardottir, HHen_US
dc.contributor.authorHaworth, Oen_US
dc.contributor.authorJones, HRen_US
dc.contributor.authorIrimia, Den_US
dc.contributor.authorSerhan, CNen_US
dc.contributor.authorPerretti, Men_US
dc.date.accessioned2016-04-22T14:32:51Z
dc.date.available2016-03-22en_US
dc.date.issued2016-04-21en_US
dc.date.submitted2016-04-15T12:39:16.368Z
dc.identifier.issn2379-3708en_US
dc.identifier.urihttp://qmro.qmul.ac.uk/xmlui/handle/123456789/12017
dc.description.abstractRheumatoid arthritis (RA) is a debilitating disease characterized by persistent accumulation of leukocytes within the articular cavity and synovial tissue. Metabololipidomic profiling of arthritic joints from omega-3 supplemented mice identified elevated levels of specialized proresolving lipid mediators (SPM) including resolvin D1 (RvD1). Profiling of human RA synovial fluid revealed physiological levels of RvD1, which - once applied to human neutrophils - attenuated chemotaxis. These results prompted analyses of the antiarthritic properties of RvD1 in a model of murine inflammatory arthritis. The stable epimer 17R-RvD1 (100 ng/day) significantly attenuated arthritis severity, cachexia, hind-paw edema, and paw leukocyte infiltration and shortened the remission interval. Metabololipidomic profiling in arthritic joints revealed 17R-RvD1 significantly reduced PGE2 biosynthesis, while increasing levels of protective SPM. Molecular analyses indicated that 17R-RvD1 enhanced expression of genes associated with cartilage matrix synthesis, and direct intraarticular treatment induced chondroprotection. Joint protective actions of 17R-RvD1 were abolished in RvD1 receptor-deficient mice termed ALX/fpr2/3-/- . These investigations open new therapeutic avenues for inflammatory joint diseases, providing mechanistic substance for the benefits of omega-3 supplementation in RA.en_US
dc.format.extente85922 - ?en_US
dc.languageengen_US
dc.language.isoenen_US
dc.relation.ispartofJCI Insighten_US
dc.rightsCC-BY
dc.titleProresolving and cartilage-protective actions of resolvin D1 in inflammatory arthritis.en_US
dc.typeArticle
dc.rights.holder© 2016 Norling et al.
dc.identifier.doi10.1172/jci.insight.85922en_US
pubs.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/27158677en_US
pubs.issue5en_US
pubs.notesNot knownen_US
pubs.notesThere is also Sarah Headland on the paper who works at QMUL. Forgot to add her. In terms of grants linked to the publication, there Dr Norling Arthritis Research UK Fellowship 19909 and Dr Headland Arthritis Research UK Fellowship 20842en_US
pubs.organisational-group/Queen Mary University of London
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry/William Harvey Research Institute
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry/William Harvey Research Institute/Biochemical Pharmacology
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry/William Harvey Research Institute/REF William Harvey Research Institute
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry/William Harvey Research Institute/William Harvey - Research Students
pubs.organisational-group/Queen Mary University of London/Faculty Reporting - Research Students
pubs.organisational-group/Queen Mary University of London/Faculty Reporting - Research Students/Faculty of Medicine & Dentistry PGRs
pubs.organisational-group/Queen Mary University of London/REF
pubs.organisational-group/Queen Mary University of London/REF/REF - UoA 01
pubs.publication-statusPublisheden_US
pubs.volume1en_US
qmul.funderThe patho-physiology of the ALX receptor in inflammation::Wellcome Trusten_US
qmul.funderThe patho-physiology of the ALX receptor in inflammation::Wellcome Trusten_US
qmul.funderThe patho-physiology of the ALX receptor in inflammation::Wellcome Trusten_US


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