Peroxiredoxin 2 overexpression protects cortical neuronal cultures from ischemic and oxidative injury but not glutamate excitotoxicity, whereas Cu/Zn superoxide dismutase 1 overexpression protects only against oxidative injury

被引:49
作者
Boulos, Sherif
Meloni, Bruno P.
Arthur, Peter G.
Bojarski, Christina
Knuckey, Neville W.
机构
[1] Univ Western Australia, QEII Med Ctr, Australian Neuromuscular Res Inst, Ctr Neuromuscular & Neurol Disorders, Nedlands, WA 6009, Australia
[2] Univ Western Australia, Sch Biomed & Chem Sci, Nedlands, WA 6009, Australia
[3] Sir Charles Gairdner Hosp, Dept Neurosurg, Nedlands, WA 6009, Australia
关键词
neuroprotection; cumene hydroperoxide; oxygen-glucose deprivation; in vitro; adenovirus;
D O I
10.1002/jnr.21429
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We previously reported that peroxiredoxin 2 (PRDX2) and Cu/Zn superoxide dismutase 1 (SOD1) proteins are up-regulated in rat primary neuronal cultures following erythropoietin (EPO) preconditioning. In the present study, we have demonstrated that adenovirally mediated overexpression of PRDX2 in cortical neuronal cultures can protect neurons from in vitro ischemia (oxygen-glucose deprivation) and an oxidative insult (cumene hydroperoxide) but not glutamate excitotoxicity. We have also demonstrated that adenovirally mediated overexpression of SOD1 in cortical neuronal cultures protected neurons only against the oxidative insult. Interestingly, we did not detect up-regulation of PRDX2 or SOD1 protein in the rat hippocampus following exposure to either 3 min or 8 min of global cerebral ischemia. Further characterization of PRDX2's neuroprotective mechanisms may aid in the development of a neuroprotective therapy. (c) 2007 Wiley-Liss, Inc.
引用
收藏
页码:3089 / 3097
页数:9
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