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@ARTICLE{Ladwig:838849,
      author       = {Ladwig, Anne and Walter, Helene Luise and Hucklenbroich,
                      Jörg and Willuweit, Antje and Langen, Karl-Josef and Fink,
                      Gereon Rudolf and Rueger, Maria Adele and Schroeter,
                      Michael},
      title        = {{O}steopontin {A}ugments {M}2 {M}icroglia {R}esponse and
                      {S}eparates {M}1- and {M}2-{P}olarized {M}icroglial
                      {A}ctivation in {P}ermanent {F}ocal {C}erebral {I}schemia},
      journal      = {Mediators of inflammation},
      volume       = {2017},
      number       = {Article ID 7189421},
      issn         = {1466-1861},
      address      = {Sylvania, Ohio},
      publisher    = {Hindawi Publishing Corp.},
      reportid     = {FZJ-2017-07359},
      pages        = {11 pages},
      year         = {2017},
      abstract     = {Background. Focal cerebral ischemia induces distinct
                      neuroinflammatory processes. We recently reported the
                      extracellular phosphor-glyco-protein osteopontin (OPN) to
                      directly affect primary microglia in vitro, promoting
                      survival while shifting their inflammatory profile towards a
                      more neutral phenotype. We here assessed the effects of OPN
                      on microglia after stroke in vivo, with focus on infarct
                      demarcation. Methods. Animals underwent focal
                      photothrombotic stroke and were injected
                      intracerebroventricularly with 500 μg OPN or vehicle.
                      Immunohistochemistry assessed neuronal damage and infarct
                      volume, neovascularisation, glial scar formation, microglial
                      activation, and M1 and M2 polarisation. Results. After
                      photothrombotic stroke, areas covered by M1 and M2 microglia
                      substantially overlapped. OPN treatment reduced that
                      overlap, with microglia appearing more spread out and
                      additionally covering the infarct core. OPN additionally
                      modulated the quantity of microglia subpopulations, reducing
                      iNOS+ M1 cells while increasing M2 microglia, shifting the
                      M1/M2 balance towards an M2 phenotype. Moreover, OPN
                      polarized astrocytes towards the infarct. Conclusion.
                      Microglial activation and M1 and M2 polarization have
                      distinct but overlapping spatial patterns in permanent focal
                      ischemia. Data suggest that OPN is involved in separating M1
                      and M2 subpopulations, as well as in shifting microglia
                      polarization towards the M2 phenotype modulating
                      beneficially inflammatory responses after focal infarction.},
      cin          = {INM-3 / INM-4 / JARA-BRAIN},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406 / I:(DE-Juel1)INM-4-20090406 /
                      $I:(DE-82)080010_20140620$},
      pnm          = {573 - Neuroimaging (POF3-573)},
      pid          = {G:(DE-HGF)POF3-573},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000411709500001},
      pubmed       = {pmid:29104378},
      doi          = {10.1155/2017/7189421},
      url          = {https://juser.fz-juelich.de/record/838849},
}