The stress gene response in brain.

S M Massa, R A Swanson, F R Sharp
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Abstract

Changes in gene expression in the brain in response to adverse conditions, such as ischemia or excitotoxin exposure, may be part of the injury process or represent an adaptive response which may be protective during subsequent stressful events. In this review we have considered the regulation, functions and potential relationships to the pathophysiology of ischemia of several major groups of stress-induced genes, including those of the M(r) 27,000, 32,000 (heme oxygenase), 70,000 and 90,000 heat shock protein families, the glucose-regulated proteins, glucose transporters and ubiquitin. Patterns of gene expression in several injury models, including focal and global ischemia, excitotoxin/ seizure-related injury and hyperthermia are reviewed. In vitro expression studies and the phenomenon of ischemic tolerance are also discussed. It is concluded that stress gene expression provides a useful marker of cellular injury, and that disjunction of mRNA and protein expression may be indicative of imminent death in cells which survive the initial insult. Though other stress proteins may play a role, it seems unlikely that neuronal hsp70 expression is a major contributor to ischemic tolerance.

大脑中的应激基因反应。
大脑中对不利条件(如缺血或兴奋毒素暴露)的基因表达变化可能是损伤过程的一部分,也可能是一种适应性反应,在随后的应激事件中具有保护作用。在这篇综述中,我们考虑了几个主要的应激诱导基因群的调控、功能及其与缺血病理生理的潜在关系,包括M(r) 27,000, 32,000(血红素加氧酶),70,000和90,000热休克蛋白家族,葡萄糖调节蛋白,葡萄糖转运蛋白和泛素。本文综述了几种损伤模型中的基因表达模式,包括局灶性和全局性缺血,兴奋毒素/癫痫相关损伤和热疗。体外表达研究和缺血耐受现象也进行了讨论。由此得出结论,应激基因的表达是细胞损伤的一个有用的标志,mRNA和蛋白表达的分离可能表明在最初的损伤中存活下来的细胞即将死亡。虽然其他应激蛋白可能起作用,但神经元hsp70的表达似乎不太可能是缺血耐受的主要贡献者。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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