[Gene expression in brain ischemia].
Ischemic stress can induce the expression of selective gene in the brain. In the acute phase of ischemia, immediate early gene is induced, and this is followed by the induction of heat shock proteins, apoptosis-related genes and inflammatory cytokines. Some of the genes expressed in the neuron induce neuronal death while other genes are related to neuronal survival. In the later phase of ischemia, genes related to neurogenesis and tissue remodeling are expressed in the brain. These genes may play an important role in the recovery of neurological function. Many of these genes are expressed mainly in the glial cells in this phase. Ischemic tolerance is powerful protective mechanism phenomenon against ischemic injury. Ischemic tolerance is induced 24-48 hours following sublethal ischemia. Since gene expression is altered during this period, gene expression may be involved in ischemic tolerance. It was reported that induction of favorable gene, such as those for heat shock proteins, might be a molecular mechanism playing some part in ischemic tolerance. On the other hand, DNA microarray analysis reveals that gene suppression, rather than expression, may play an important role in the molecular mechanism underlying ischemic tolerance. Gene expression profiles in ischemic brain and in ischemic tolerance have been investigated and a part of the molecular mechanism involved in those phenomena has been revealed recently. Although further study is necessary, gene expression may be an important therapeutic target in ischemic stroke.
Yagita
Yoshiki
Y
Department of Neurology, Osaka University Graduate School of Medicine, 2 2 Yamadaoka, Suita-shi, Osaka 565-0871, Japan.
Sakoda
Saburo
S
Kitagawa
Kazuo
K
D051017:Apoptosis Regulatory Proteins; D002545:Brain Ischemia / Q000235:genetics*; D016923:Cell Death; D002470:Cell Survival / Q000235:genetics; D016207:Cytokines; D015870:Gene Expression; D020869:Gene Expression Profiling; D017781:Genes, Immediate-Early; D006360:Heat-Shock Proteins; D006801:Humans; D018836:Inflammation Mediators; D019194:Ischemic Preconditioning; D009457:Neuroglia; D014157:Transcription Factors; D015533:Transcriptional Activation
D051017:Apoptosis Regulatory Proteins; D016207:Cytokines; D006360:Heat-Shock Proteins; D018836:Inflammation Mediators; D014157:Transcription Factors