CREB is required for acquisition of ischemic tolerance in gerbil hippocampal CA1 region

被引:82
作者
Hara, T [1 ]
Hamada, J [1 ]
Yano, S [1 ]
Morioka, M [1 ]
Kai, Y [1 ]
Ushio, Y [1 ]
机构
[1] Kumamoto Univ, Sch Med, Dept Neurosurg, Kumamoto 8608556, Japan
关键词
CRE decoy oligonucleotide; cyclic AMP responsive element binding protein; gerbil; hippocampus; ischemic tolerance; ELEMENT-BINDING PROTEIN; DECOY OLIGONUCLEOTIDE; CEREBRAL-ISCHEMIA; GENE-EXPRESSION; NEURONAL DEATH; TRANSCRIPTION; PHOSPHORYLATION; BRAIN; RAT; ACTIVATION;
D O I
10.1046/j.1471-4159.2003.01847.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ischemic tolerance is well known as a neuroprotective effect of pre-conditioning ischemia against delayed neuronal death, however, the mechanism or mechanisms underlying this effect are not fully understood. We investigated the relationship between CREB and ischemic tolerance in gerbil hippocampal CA1 neurons using CRE decoy oligonucleotide. Sublethal ischemia led to an increase in the level of CREB phosphorylation in CA1 regions while lethal ischemia did not. Experiments with NG108-15 cells showed that adding CRE decoy oligonucleotide to culture media significantly inhibited the cell growth rate. The administration of CRE decoy oligonucleotide into gerbil cerebral ventricle decreased CREB-DNA binding activity to 38% of the control. Pre-treatment with CRE decoy oligonucleotide 24 h before the induction of ischemic tolerance decreased CA1 neuronal cell survival to 21% of the control. The present findings suggest that a CREB-mediated transcription system is necessary for the induction of ischemic tolerance.
引用
收藏
页码:805 / 814
页数:10
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