The superoxide dismutase1 (SOD1) G93A mutation does not promote neuronal injury after focal brain ischemia and optic nerve transection in mice

被引:4
作者
Kilic, E
Weishaupt, JH
Kilic, Ü
Rohde, G
Yulug, B
Peters, K
Hermann, DM
Bähr, M
机构
[1] Univ Hosp Zurich, Dept Neurol, CH-8091 Zurich, Switzerland
[2] Univ Hosp Gottingen, Dept Neurol, D-37075 Gottingen, Germany
关键词
free radical scavenging; oxidative stress; ischemic stroke; familial amyotrophic lateral sclerosis;
D O I
10.1016/j.neuroscience.2004.06.064
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The superoxide dismutase 1 (SOD1) G93A mouse was recently established as transgenic model of amyotrophic lateral sclerosis. We were interested to know whether the SOD1 G93A mutation promotes neuronal injury after intraluminal middle cerebral artery thread occlusion and/or retinal ganglion cell (RGC) axotomy in mice, which are highly reproducible and clinically relevant in vivo models of acute and subacute neuronal degeneration, respectively. In our experiments, G93A mutant SOD1 neither influenced ischemic injury after 90 or 30 min of focal ischemia, nor had an impact on the severity of RGC degeneration after optic nerve transection, when human SOD1 G93A mutant mice were compared to human wild-type SOD1 mice. Our data indicate that the clinically relevant SOD1 G93A mutation, which leads to amyotrophic lateral sclerosis in humans and mice, does not necessarily worsen neuronal degeneration in other pathologies. Thus, the G93A mutation may be counterbalanced in non-motor neurons of young animals, and region-specific and age-related factors may be necessary so that neurodegeneration is re-enforced. (C) 2004 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:359 / 364
页数:6
相关论文
共 29 条
[1]   Reactive oxygen radicals in signaling and damage in the ischemic brain [J].
Chan, PH .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2001, 21 (01) :2-14
[2]   Cu,Zn-superoxide dismutase-dependent apoptosis induced by nitric oxide in neuronal cells [J].
Ciriolo, MR ;
De Martino, A ;
Lafavia, E ;
Rossi, L ;
Carrí, MT ;
Rotilio, G .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (07) :5065-5072
[3]  
Dunlop J, 2003, J NEUROSCI, V23, P1688
[4]  
Facchinetti F, 1998, CELL MOL NEUROBIOL, V18, P667, DOI 10.1023/A:1020221919154
[5]   MOTOR-NEURON DEGENERATION IN MICE THAT EXPRESS A HUMAN CU,ZN SUPEROXIDE-DISMUTASE MUTATION [J].
GURNEY, ME ;
PU, HF ;
CHIU, AY ;
DALCANTO, MC ;
POLCHOW, CY ;
ALEXANDER, DD ;
CALIENDO, J ;
HENTATI, A ;
KWON, YW ;
DENG, HX ;
CHEN, WJ ;
ZHAI, P ;
SUFIT, RL ;
SIDDIQUE, T .
SCIENCE, 1994, 264 (5166) :1772-1775
[6]   Dynamics of regional brain metabolism and gene expression after middle cerebral artery occlusion in mice [J].
Hata, R ;
Maeda, K ;
Hermann, D ;
Mies, G ;
Hossmann, KA .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2000, 20 (02) :306-315
[7]   Adenovirus-mediated GDNF and CNTF pretreatment protects against striatal injury following transient middle cerebral artery occlusion in mice [J].
Hermann, DM ;
Kilic, E ;
Kügler, S ;
Isenmann, S ;
Bähr, M .
NEUROBIOLOGY OF DISEASE, 2001, 8 (04) :655-666
[8]   Relationship between metabolic dysfunctions, gene responses and delayed cell death after mild focal cerebral ischemia in mice [J].
Hermann, DM ;
Kilic, E ;
Hata, R ;
Hossmann, KA ;
Mies, G .
NEUROSCIENCE, 2001, 104 (04) :947-955
[9]   Focal loss of the glutamate transporter EAAT2 in a transgenic rat model of SOD1 mutant-mediated amyotrophic lateral sclerosis (ALS) [J].
Howland, DS ;
Liu, J ;
She, YJ ;
Goad, B ;
Maragakis, NJ ;
Kim, B ;
Erickson, J ;
Kulik, J ;
DeVito, L ;
Psaltis, G ;
DeGennaro, LJ ;
Cleveland, DW ;
Rothstein, JD .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (03) :1604-1609
[10]   Age-related changes in peroxisomal membrane protein 70 and superoxide dismutase 1 in transgenic G93A mice [J].
Ilieva, HS ;
Nagano, I ;
Murakami, T ;
Shiote, M ;
Manabe, Y ;
Abe, K .
NEUROLOGICAL RESEARCH, 2003, 25 (04) :423-426