Abstract
Cells in brain and other tissues respond to ischemic insults with diverse changes in gene expression. The distribution and cellular specificity of such responses in brain differ considerably after global and focal ischemia and are strongly dependent on the duration and severity of blood flow deficits. This review initially focuses on inducible transcription factors encoded by cellular immediate-early genes (cIEGs) of the fos/jun/krox multigene families, and the stress protein, hsp72, which is the most thoroughly studied member of the 70-kDa heat shock protein family in the central nervous system (CNS). It will be demonstrated that induction of cIEGs constitutes a lowthreshold response to brief depolarization, whereas hsp72 induction is more closely associated with potentially injurious stimuli in both global and focal ischemia models. Discrepancies between patterns of mRNA and protein expression will demonstrate the influence of postischemic protein synthesis deficits on mRNA translation. Within this framework, consideration will then be given to other ischemia-induced gene products, including other transcription factors and stress proteins, as well as neurotrophic factors, components of oxidative defense mechanisms, and gene products thought to be involved in regulating cell death. Emphasis is placed on neuronal gene expression, as changes in other cell types may be viewed as components of reactive responses considered in Chapters 9 and 10. A recent review provides a compact summary of postischemic changes in gene expression that may complement this presentation (Koistinaho and Hökfelt, 1997).
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Nowak, T.S., Kiessling, M. (1999). Reprogramming of Gene Expression After Ischemia. In: Walz, W. (eds) Cerebral Ischemia. Contemporary Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-479-5_7
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