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@ARTICLE{Claus:201376,
      author       = {Claus, Helene L. and Walberer, Maureen and Simard, Marie L.
                      and Emig, Beata and Muesken, Sophia M. and Rueger, Maria A.
                      and Fink, Gereon R. and Schroeter, Michael},
      title        = {{NG}2 and {NG}2-positive cells delineate focal cerebral
                      infarct demarcation in rats},
      journal      = {Neuropathology},
      volume       = {33},
      number       = {1},
      issn         = {0919-6544},
      address      = {Oxford [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {FZJ-2015-03671},
      pages        = {30 - 38},
      year         = {2013},
      abstract     = {Focal cerebral ischemia induces cellular responses that may
                      result in secondary tissue damage. We recently demonstrated
                      multi-facetted spatial and temporal patterns of
                      neuroinflammation by multimodal imaging. In the present
                      study, we especially focus on the separation of vital and
                      necrotic tissue, which enabled us to define a demarcation
                      zone. Focal cerebral ischemia was induced via macrosphere
                      embolization of the middle cerebral artery in Wistar rats.
                      Subsequent cellular processes were investigated
                      immunohistochemically from 3 to 56 days after onset of
                      ischemia. We detected several infarct subareas: a necrotic
                      infarct core and its margin adjacent to a nerve/glial
                      antigen 2 (NG2)+ zone delineating it from a vital
                      peri-infarct zone. Initially transition from necrotic to
                      vital tissue was gradual; later on necrosis was precisely
                      separated from vital tissue by a narrow NG2+ belt that was
                      devoid of astrocytes, oligodendrocytes or neurons. Within
                      this demarcation zone NG2+ cells associate with ionized
                      calcium binding adaptor molecule 1 (Iba1) but not with GFAP,
                      neuronal nuclear antigen (NeuN) or 2′, 3′-cyclic
                      nucleotide 3′-phosphodiesterase (CNPase). During further
                      infarct maturation NG2 seemed to be positioned in the
                      extracellular matrix (ECM) of the demarcation zone, whereas
                      Iba1+ cells invaded the necrotic infarct core and GFAP+
                      cells built a gliotic containing belt between the lesion and
                      NeuN+ unaffected tissue. Overall, our data suggested that
                      NG2 proteoglycan expression and secretion hallmarked
                      demarcation as a process that actively separated necrosis
                      from vital tissue and therefore decisively impacts secondary
                      neurodegeneration after ischemic stroke.},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {333 - Pathophysiological Mechanisms of Neurological and
                      Psychiatric Diseases (POF2-333)},
      pid          = {G:(DE-HGF)POF2-333},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000314472000004},
      doi          = {10.1111/j.1440-1789.2012.01322.x},
      url          = {https://juser.fz-juelich.de/record/201376},
}