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dc.contributor.authorRao, Sindhuja M
dc.contributor.authorAuger, Jennifer L
dc.contributor.authorGaillard, Philippe
dc.contributor.authorWeissleder, Ralph
dc.contributor.authorWada, Etsuko
dc.contributor.authorTorres, Richard
dc.contributor.authorKojima, Masayasu
dc.contributor.authorBenoist, Christophe O.
dc.contributor.authorMathis, Diane J.
dc.contributor.authorBinstadt, Bryce A
dc.date.accessioned2013-03-21T20:31:18Z
dc.date.issued2012
dc.identifier.citationRao, Sindhuja M, Jennifer L Auger, Philippe Gaillard, Ralph Weissleder, Etsuko Wada, Richard Torres, Masayasu Kojima, Christophe Benoist, Diane Mathis, and Bryce A Binstadt. 2012. The neuropeptide neuromedin U promotes autoantibody-mediated arthritis. Arthritis Research & Therapy 14(1): R29.en_US
dc.identifier.issn1478-6354en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:10456178
dc.description.abstractIntroduction: Neuromedin U (NMU) is a neuropeptide with pro-inflammatory activity. The primary goal of this study was to determine if NMU promotes autoantibody-induced arthritis. Additional studies addressed the cellular source of NMU and sought to define the NMU receptor responsible for its pro-inflammatory effects. Methods: Serum containing arthritogenic autoantibodies from K/BxN mice was used to induce arthritis in mice genetically lacking NMU. Parallel experiments examined whether NMU deficiency impacted the early mast-cell-dependent vascular leak response induced by these autoantibodies. Bone-marrow chimeric mice were generated to determine whether pro-inflammatory NMU is derived from hematopoietic cells or stromal cells. Mice lacking the known NMU receptors singly and in combination were used to determine susceptibility to serum-transferred arthritis and in vitro cellular responses to NMU. Results: NMU-deficient mice developed less severe arthritis than control mice. Vascular leak was not affected by NMU deficiency. NMU expression by bone-marrow-derived cells mediated the pro-arthritogenic effect. Deficiency of all of the known NMU receptors, however, had no impact on arthritis severity and did not affect the ability of NMU to stimulate intracellular calcium flux. Conclusions: NMU-deficient mice are protected from developing autoantibody-induced inflammatory arthritis. NMU derived from hematopoietic cells, not neurons, promotes the development of autoantibody-induced inflammatory arthritis. This effect is mediated by a receptor other than the currently known NMU receptors.en_US
dc.language.isoen_USen_US
dc.publisherBioMed Centralen_US
dc.relation.isversionofdoi:10.1186/ar3732en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3392824/pdf/en_US
dash.licenseLAA
dc.titleThe neuropeptide neuromedin U promotes autoantibody-mediated arthritisen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalArthritis Research & Therapyen_US
dash.depositing.authorBenoist, Christophe O.
dc.date.available2013-03-21T20:31:18Z
dc.identifier.doi10.1186/ar3732*
dash.contributor.affiliatedMathis, Diane
dash.contributor.affiliatedBenoist, Christophe
dash.contributor.affiliatedWeissleder, Ralph


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