Induction of heat shock protein 40 and GrpE mRNAs following transient focal cerebral ischemia in the rat

Tamura, Shun; Kinouchi, Hiroyuki; Izaki, Kenji; Okubo, Atsuya; Sugawara, Taku; Kunizuka, Hisanori; Mizoi, Kazuo

doi:10.1016/s0006-8993(02)03887-8

Cited by 2 publications

(1 citation statement)

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“…In this study, the expression of Hsp40 is increased. The induction of Hsp40 mRNA has also been demonstrated after focal transient cerebral ischemia (Paschen et al, 1998;Tamura et al, 2003;Tanaka et al, 2002). Hsp40 has been shown to interact with and regulate the ATPase activity of Hsp70 (Naylor et al, 1998) and Hsp70-Hsp40 chaperone pairs have been shown to prevent nitric oxide-mediated apoptosis in macrophages (Gotoh et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

DNA Microarray Analysis of Hippocampal Gene Expression Measured Twelve Hours after Hypoxia-Ischemia in the Mouse

Gilbert

Costain

Blanchard

et al. 2003

J Cereb Blood Flow Metab

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Summary:Cell death from cerebral ischemia is a dynamic process. In the minutes to days after an ischemic insult, progressive changes in cellular morphology occur. Associated with these events is the regulation of competing programs of gene expression; some are protective against ischemic insult, and others contribute to delayed cell death. Many genes involved in these processes have been identified, but individually, these findings have provided only limited insight into the systems biology of cerebral ischemia. Attempts to characterize the coordinated expression of large numbers of genes in cerebral ischemia has only recently become possible. Today, DNA microarray technology provides a powerful tool for investigating parallel expression changes for thousands of genes at one time.In this study, adult mice were subjected to 30 minutes of hypoxia-ischemia (HI), and the hippocampus was examined 12 hours later for differential gene expression using a 15K highdensity mouse EST array. The genomic response to HI is complex, affecting approximately 7% of the total number of ESTs examined. Assigning differentially expressed ESTs to molecular functional groups revealed that HI affects many pathways including the molecular chaperones, transcription factors, kinases, and calcium ion binding genes. A comprehensive list of regulated genes should prove valuable in advancing our understanding of the pathogenesis of cerebral ischemia.

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