Cu-II(atsm) Attenuates Neuroinflammation

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dc.contributor.author Choo, Xin Yi
dc.contributor.author Liddell, Jeffrey R.
dc.contributor.author Huuskonen, Mikko T.
dc.contributor.author Grubman, Alexandra
dc.contributor.author Moujalled, Diane
dc.contributor.author Roberts, Jessica
dc.contributor.author Kysenius, Kai
dc.contributor.author Patten, Lauren
dc.contributor.author Quek, Hazel
dc.contributor.author Oikari, Lotta E.
dc.contributor.author Duncan, Clare
dc.contributor.author James, Simon A.
dc.contributor.author McInnes, Lachlan E.
dc.contributor.author Hayne, David J.
dc.contributor.author Donnelly, Paul S.
dc.contributor.author Pollari, Eveliina
dc.contributor.author Vähätalo, Suvi
dc.contributor.author Lejavova, Katarina
dc.contributor.author Kettunen, Mikko
dc.contributor.author Malm, Tarja
dc.contributor.author Koistinaho, Jari
dc.contributor.author White, Anthony R.
dc.contributor.author Kanninen, Katja M.
dc.date.accessioned 2018-10-09T09:02:01Z
dc.date.available 2018-10-09T09:02:01Z
dc.date.issued 2018-09-24
dc.identifier.citation Choo , X Y , Liddell , J R , Huuskonen , M T , Grubman , A , Moujalled , D , Roberts , J , Kysenius , K , Patten , L , Quek , H , Oikari , L E , Duncan , C , James , S A , McInnes , L E , Hayne , D J , Donnelly , P S , Pollari , E , Vähätalo , S , Lejavova , K , Kettunen , M , Malm , T , Koistinaho , J , White , A R & Kanninen , K M 2018 , ' Cu-II(atsm) Attenuates Neuroinflammation ' , Frontiers in Neuroscience , vol. 12 , 668 . https://doi.org/10.3389/fnins.2018.00668
dc.identifier.other PURE: 116612703
dc.identifier.other PURE UUID: 8e141d6c-171f-4760-b050-f77ef2311a5a
dc.identifier.other WOS: 000445368300001
dc.identifier.other Scopus: 85055162725
dc.identifier.other ORCID: /0000-0001-6559-1153/work/53186000
dc.identifier.uri http://hdl.handle.net/10138/248084
dc.description.abstract Background: Neuroinflammation and biometal dyshomeostasis are key pathological features of several neurodegenerative diseases, including Alzheimer's disease (AD). Inflammation and biometals are linked at the molecular level through regulation of metal buffering proteins such as the metallothioneins. Even though the molecular connections between metals and inflammation have been demonstrated, little information exists on the effect of copper modulation on brain inflammation. Methods: We demonstrate the immunomodulatory potential of the copper bis(thiosemicarbazone) complex Cu-II(atsm) in an neuroinflammatory model in vivo and describe its anti-inflammatory effects on microglia and astrocytes in vitro. Results: By using a sophisticated in vivo magnetic resonance imaging (MRI) approach, we report the efficacy of Cu-II(atsm) in reducing acute cerebrovascular inflammation caused by peripheral administration of bacterial lipopolysaccharide (LPS). Cu-II(atsm) also induced anti-inflammatory outcomes in primary microglia [significant reductions in nitric oxide (NO), monocyte chemoattractant protein 1 (MCP-1), and tumor necrosis factor (TNF)] and astrocytes [significantly reduced NO, MCP-1, and interleukin 6 (IL-6)] in vitro. These anti-inflammatory actions were associated with increased cellular copper levels and increased the neuroprotective protein metallothionein-1 (MT1) in microglia and astrocytes. Conclusion: The beneficial effects of Cu-II(atsm) on the neuroimmune system suggest copper complexes are potential therapeutics for the treatment of neuroinflammatory conditions. en
dc.format.extent 14
dc.language.iso eng
dc.relation.ispartof Frontiers in Neuroscience
dc.rights.uri info:eu-repo/semantics/openAccess
dc.subject microglia
dc.subject astrocyte
dc.subject inflammation
dc.subject neurodegeneration
dc.subject copper
dc.subject AMYOTROPHIC-LATERAL-SCLEROSIS
dc.subject PLASMA-MASS SPECTROMETRY
dc.subject METALLOTHIONEIN GENE-EXPRESSION
dc.subject AMYLOID-BETA PEPTIDE
dc.subject ALZHEIMERS-DISEASE
dc.subject MOUSE MODEL
dc.subject MICROGLIAL ACTIVATION
dc.subject ANIMAL-MODELS
dc.subject IN-VIVO
dc.subject INFLAMMATORY RESPONSES
dc.subject 3112 Neurosciences
dc.subject 3124 Neurology and psychiatry
dc.title Cu-II(atsm) Attenuates Neuroinflammation en
dc.type Article
dc.contributor.organization Neuroscience Center
dc.contributor.organization University of Helsinki
dc.description.reviewstatus Peer reviewed
dc.relation.doi https://doi.org/10.3389/fnins.2018.00668
dc.relation.issn 1662-453X
dc.rights.accesslevel openAccess
dc.type.version publishedVersion

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