Increased expression of apoptosis-linked gene 2 (ALG2) in the rat brain after temporary focal cerebral ischemia

被引:23
作者
Li, W
Jin, K [1 ]
Nagayama, T
He, X
Chang, J
Minami, M
Graham, SH
Simon, RP
Greenberg, DA
机构
[1] Buck Ctr Res Aging, Novato, CA 94948 USA
[2] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15261 USA
关键词
apoptosis-linked gene 2; cerebral ischemia; apoptosis; programmed cell death; gene expression;
D O I
10.1016/S0306-4522(99)00531-X
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Calcium is an important mediator of programmed cell death induced by transient cerebral ischemia, and calcium-binding proteins have been implicated in calcium-regulated signal transduction. Apoptosis-linked gene 2 is a calcium-binding protein required for cell death induced by different apoptotic stimuli. By Western blot analysis, we found that apoptosis-linked gene 2 protein was expressed in normal brains, and that expression increased in ischemic brains after 20 or 90 min of transient focal cerebral ischemia. Immunocytochemistry showed increased apoptosis-linked gene 2 protein expression in frontal cortex, a region where neurons underwent ischemic stress but still survived, after 20 or 90 min of focal cerebral ischemia. Apoptosis-linked gene 2 protein was also up-regulated in the ischemic border-zone of parietal cortex 24 h after 20 min of focal ischemia, and was remarkably over-expressed in the caudate-putamen and parietal cortex, (where cells are destined to die) 24 h after 90 min of ischemia. The expression pattern of apoptosis-linked gene 2 protein was similar to that of deoxyribonucleic acid damage detected by Klenow labeling assay. Our results suggest that apoptosis-linked gene 2 may be involved in the regulation of cell death after transient focal cerebral ischemia. (C) 2000 IBRO. Published by Elsevier Science Ltd.
引用
收藏
页码:161 / 168
页数:8
相关论文
共 23 条
[1]   Mechanisms of neuronal damage in brain hypoxia/ischemia: Focus on the role of mitochondrial calcium accumulation [J].
Budd, SL .
PHARMACOLOGY & THERAPEUTICS, 1998, 80 (02) :203-229
[2]  
Chen J, 1998, J NEUROSCI, V18, P4914
[3]  
COHEN JJ, 1984, J IMMUNOL, V132, P38
[4]   Focal ischemia induces expression of the DNA damage-inducible gene GADD45 in the rat brain [J].
Jin, KL ;
Chen, J ;
Kawaguchi, K ;
Zhu, RL ;
Stetler, RA ;
Simon, RP ;
Graham, SH .
NEUROREPORT, 1996, 7 (11) :1797-1802
[5]   In situ detection of neuronal DNA strand breaks using the Klenow fragment of DNA polymerase I reveals different mechanisms of neuron death after global cerebral ischemia [J].
Jin, KL ;
Chen, J ;
Nagayama, T ;
Chen, MZ ;
Sinclair, J ;
Graham, SH ;
Simon, RP .
JOURNAL OF NEUROCHEMISTRY, 1999, 72 (03) :1204-1214
[6]   Ca2+ channel antagonists and neuroprotection from cerebral ischemia [J].
Kobayashi, T ;
Mori, Y .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1998, 363 (01) :1-15
[7]  
Lacana E, 1997, J IMMUNOL, V158, P5129
[8]   Synergistic effects of caspase inhibitors and MK-801 in brain injury after transient focal cerebral ischaemia in mice [J].
Ma, JY ;
Endres, M ;
Moskowitz, MA .
BRITISH JOURNAL OF PHARMACOLOGY, 1998, 124 (04) :756-762
[9]   Calcium-induced exposure of a hydrophobic surface of mouse ALG-2, which is a member of the penta-EF-hand protein family [J].
Maki, M ;
Yamaguchi, K ;
Kitaura, Y ;
Satoh, H ;
Hitomi, K .
JOURNAL OF BIOCHEMISTRY, 1998, 124 (06) :1170-1177
[10]  
Maki M, 1997, BIOCHEM J, V328, P718