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

Abstract

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.

Gene Expression Profiles in Hypoxic Preconditioning Using Cdna Microarray Analysis: Altered Expression of an Angiogenic Factor, Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1

“…Today, cDNA microarray technology provides a powerful tool for investigating parallel expression changes for thousands of genes at one time. Several microarray approaches have been tried in different hypoxic systems, including hypoxic lung, endothelial cells, fibroblasts, breast cancer cells (MCF-7 and MDA-MB-231), cerebral cortical neurons, hippocampus, and zebrafish exposed to hypoxia (8)(9)(10). However, to the best of our knowledge, the gene expression profile of hypoxia preconditioning in heart has not been identified.…”

Help-me signaling: Non-cell autonomous mechanisms of neuroprotection and neurorecovery

“…Microarray studies investigating the transcriptome of both focal and global ischemia showed that the differentially expressed genes involved immediate early genes, stress response genes, apoptosis, signal transduction, neurotransmission, ion channels, inflammation, cytoskeleton, ribosome, and neurotrophic factors, et al (Buttner et al 2009; Cox-Limpens et al 2014; Gilbert et al 2003; Hori et al 2012; Jin et al 2001b; Lu et al 2003; Lu et al 2004; Ramos-Cejudo et al 2012; Sarabi et al 2008; Schmidt-Kastner et al 2002; Soriano et al 2000; Sun et al 2007; Tang et al 2002; Wang et al 2011a; Yakubov et al 2004). …”

Global Gene Expression in the Immature Brain after Hypoxia-Ischemia

“…Several previous studies that have investigated changes in gene expression after adult ischemia have focused on the cortex (Kim et al, 2002;Lu et al, 2003;Schmidt-Kastner et al, 2002) or hippocampus (Gilbert et al, 2003;Jin et al, 2001) only. Because the injury after neonatal HI develops in other regions as well, choosing only one specific region would potentially leave out important genes that are expressed locally in distinct areas.…”