TY  - JOUR
AU  - Claus, Helene L.
AU  - Walberer, Maureen
AU  - Simard, Marie L.
AU  - Emig, Beata
AU  - Muesken, Sophia M.
AU  - Rueger, Maria A.
AU  - Fink, Gereon R.
AU  - Schroeter, Michael
TI  - NG2 and NG2-positive cells delineate focal cerebral infarct demarcation in rats
JO  - Neuropathology
VL  - 33
IS  - 1
SN  - 0919-6544
CY  - Oxford [u.a.]
PB  - Wiley-Blackwell
M1  - FZJ-2015-03671
SP  - 30 - 38
PY  - 2013
AB  - 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.
LB  - PUB:(DE-HGF)16
UR  - <Go to ISI:>//WOS:000314472000004
DO  - DOI:10.1111/j.1440-1789.2012.01322.x
UR  - https://juser.fz-juelich.de/record/201376
ER  -