scholarly journals Copper/Zinc Superoxide Dismutase Attenuates Neuronal Cell Death by Preventing Extracellular Signal-Regulated Kinase Activation after Transient Focal Cerebral Ischemia in Mice

2002 ◽  
Vol 22 (18) ◽  
pp. 7923-7930 ◽  
Author(s):  
Nobuo Noshita ◽  
Taku Sugawara ◽  
Takeshi Hayashi ◽  
Anders Lewén ◽  
Ghezal Omar ◽  
...  
Keyword(s):  
Focal Cerebral Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Kinase Activation ◽  
Copper Zinc Superoxide Dismutase ◽  
Extracellular Signal Regulated Kinase ◽  
Zinc Superoxide Dismutase ◽  
Transient Focal Cerebral Ischemia ◽  
Extracellular Signal ◽  
Copper Zinc

Correlation between copper/zinc superoxide dismutase and the proliferation of neural stem cells in aging and following focal cerebral ischemia

2006 ◽  
Vol 104 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Sunao Takemura ◽  
Takamasa Kayama ◽  
Atsushi Kuge ◽  
Hasmat Ali ◽  
Yasuaki Kokubo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Cerebral Ischemia ◽  
Transgenic Mice ◽  
Focal Cerebral Ischemia ◽  
Wild Type ◽  
Copper Zinc Superoxide Dismutase ◽  
Zinc Superoxide Dismutase ◽  
Transient Focal Cerebral Ischemia ◽  
Copper Zinc

Object Neural stem cells (NSCs) have been demonstrated in the subventricular zone (SVZ) of the lateral ventricle and the subgranular zone of the hippocampal dentate gyrus (DG). Although aging rats manifest a decrease in NSCs, rats exposed to stress (for example, ischemia, epilepsy, radiation, and trauma) show an increase in these cells. In transgenic mice, the overexpression of human copper/zinc superoxide dismutase (SOD1), an endogenous antioxidant, has been reported to be a protective enzyme against transient focal cerebral ischemia. The authors investigated the correlation between SOD1 and the proliferation of NSCs in aging as chronic oxidative stress (Experiment 1) and acute oxidative stress induced by transient focal cerebral ischemia (Experiment 2) in mice. Methods Bromodeoxyuridine (BrdU) was used in the evaluation of NSCs. In Experiment 1, NSCs in the SVZ significantly increased in 16-month-old transgenic mice compared with wild-type mice (p = 0.0001). In Experiment 2, mice were subjected to 30-minute occlusions of the middle cerebral artery. The increase in NSCs in the DG in transgenic mice was significantly greater than that in wild-type mice (p < 0.05). Conclusions Results in this study suggest that chronic and acute oxidative stress may inhibit the proliferation of NSCs and that SOD1 may play a key role in NSC proliferation.

Apoptosis inducing factor (AIF) is essential for neuronal cell death following transient focal cerebral ischemia

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S466-S466
Author(s):  
Carsten Culmsee ◽  
Changlian Zhu ◽  
Miriam Höhn ◽  
Stefan Landshamer ◽  
Uta Mamrak ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Transient Focal Cerebral Ischemia ◽  
Apoptosis Inducing Factor
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