TY - JOUR
T1 - Expression of endothelial nitric oxide synthase in the ischemic penumbra
T2 - Relationship to expression of neuronal nitric oxide synthase and vascular endothelial growth factor
AU - Leker, Ronen R.
AU - Teichner, Angella
AU - Ovadia, Haim
AU - Keshet, Eli
AU - Reinherz, Esther
AU - Ben-Hur, Tamir
PY - 2001/8/3
Y1 - 2001/8/3
N2 - Expressional patterns of the endothelial and neuronal forms of nitric oxide synthase (NOS) in cerebral ischemia were studied utilizing a permanent middle cerebral artery occlusion (PMCAO) model. Motor performance and infarct volumes were determined in the rats. Immunohistochemical staining for eNOS, nNOS and neurofilament were performed at 1, 2, 3, 5, 7 and 14 days after PMCAO. Vascular endothelial growth factor (VEGF) expression was determined by in-situ hybridization. PMCAO caused a reproducible cortical infarct with motor deficits in the rats. Double immunohistochemical stainings indicated that eNOS and nNOS were induced in ischemic neurons. Most stained neurons were positive for both NOS forms but some reacted with only one NOS antibody. nNOS expression peaked at 24-48 h after PMCAO, stained mainly the cytoplasm of core neurons, and disappeared after the 3rd day. eNOS expression increased until the 7th day, stained mainly the cytoplasm and membrane of penumbral cells and disappeared by the 14th day after PMCAO. VEGF expression was significantly induced in the penumbral zone in a similar distribution to eNOS. The anatomical and temporal pattern of VEGF and eNOS induction in the brain after permanent ischemia suggest that these mediators may play a role in protecting penumbral tissue from additional ischemic damage.
AB - Expressional patterns of the endothelial and neuronal forms of nitric oxide synthase (NOS) in cerebral ischemia were studied utilizing a permanent middle cerebral artery occlusion (PMCAO) model. Motor performance and infarct volumes were determined in the rats. Immunohistochemical staining for eNOS, nNOS and neurofilament were performed at 1, 2, 3, 5, 7 and 14 days after PMCAO. Vascular endothelial growth factor (VEGF) expression was determined by in-situ hybridization. PMCAO caused a reproducible cortical infarct with motor deficits in the rats. Double immunohistochemical stainings indicated that eNOS and nNOS were induced in ischemic neurons. Most stained neurons were positive for both NOS forms but some reacted with only one NOS antibody. nNOS expression peaked at 24-48 h after PMCAO, stained mainly the cytoplasm of core neurons, and disappeared after the 3rd day. eNOS expression increased until the 7th day, stained mainly the cytoplasm and membrane of penumbral cells and disappeared by the 14th day after PMCAO. VEGF expression was significantly induced in the penumbral zone in a similar distribution to eNOS. The anatomical and temporal pattern of VEGF and eNOS induction in the brain after permanent ischemia suggest that these mediators may play a role in protecting penumbral tissue from additional ischemic damage.
KW - Free radical
KW - Nitric oxide synthase
KW - Permanent middle cerebral artery occlusion
KW - Stroke
KW - Vascular endothelial growth factor
UR - http://www.scopus.com/inward/record.url?scp=0035800586&partnerID=8YFLogxK
U2 - 10.1016/S0006-8993(01)02561-6
DO - 10.1016/S0006-8993(01)02561-6
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C2 - 11478916
AN - SCOPUS:0035800586
SN - 0006-8993
VL - 909
SP - 1
EP - 7
JO - Brain Research
JF - Brain Research
IS - 1-2
ER -