STRESS PROTEIN INDUCTION IN BRAIN AFTER ISCHEMIA

正在进行的研究继续关注基因表达改变的作用 在缺血后病理生理学中的作用 具体而言，转录和 应激蛋白hsp 7 O的翻译表达和转录 因子Fos和Jun，通过比较原位 杂交和免疫细胞化学。 也许最重要的 结果是观察到阈值缺血，导致 诱导的对后续挑战的耐受性，与hsp 7 O相关， Jun在受保护的脆弱CA 1神经元中的表达。 蛋白 在严重初始损伤之后的合成缺陷显然导致 即使它们可能被诱导，也无法翻译mRNA。 以来 Jun反过来又调节其他转录因子的转录表达。 基因，这一发现开始表明基因的复杂性， 重编程必须与诱导耐受现象相关。 在局部缺血后已经评估了基因表达的其他变化， 特别是微管相关蛋白2（MAP-2）。 的mRNA 编码截短的蛋白质MAP-2c，在皮质中被诱导， 在大鼠心脏骤停中显示延迟损伤的海马CA 1区 模型与应激蛋白和原癌基因表达相反， MAP-2c主要发生在存活的神经元中，MAP-2c似乎构成了 缺血后严重损伤神经元的选择性标记物。

Ongoing studies continue to focus on the role of altered gene expression in postischemic patho-physiology. Specifically, transcriptional and translational expression of the stress protein, hsp7O, and transcription factors, Fos and Jun, are evaluated by comparison of in situ hybridization and immunocytochemistry. Perhaps the most significant result has been the observation that threshold ischemic , resulting in an induced tolerance to subsequent challenges, are correlated with hsp7O and Jun expression in the vulnerable CAl neurons that are protected. Protein synthesis deficits that follow severe initial insults apparently result in the failure to translate mRNAs even though they may be induced. Since Jun in turn functions to regulate the transcriptional expression of other genes, this finding begins to indicate the complexity of genetic reprogramming that must be associated with induced tolerance phenomena. Other changes in gene expression have been evaluated after ischemia, notably that of microtubule-associated protein 2 (MAP-2). An mRNA encoding a truncated protein, MAP-2c, is induced in cortex and hippocampal CAl regions that show delayed damage in a rat cardiac arrest model. in contrast to stress protein and proto-oncogene expression that largely occur in surviving neurons, MAP-2c appears to constitute a selective marker for severely injured neurons after ischemia.