DNA microarray analysis of cortical gene expression during early recirculation after focal brain ischemia in rat

Schmidt‐Kastner, Rainald; Zhang, Baotong; Belayev, Ludmila; Khoutorova, Larissa; Amin, Rupen; Busto, Raul; Ginsberg, Myron D.

doi:10.1016/s0169-328x(02)00516-8

Cited by 100 publications

(83 citation statements)

References 76 publications

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“…However, the majority studies measured gene profiles in the brain cells other than SVZ cells focusing on the acute stage of ischemic stroke (Sharp et al, 2000;Kim et al, 2002;Schmidt-Kastner et al, 2002;Lu et al, 2004;Rickhag et al, 2006). Further studies to identify genes trigged by ischemia specific for neural progenitor cells are warranted.…”

Section: Discussionmentioning

confidence: 99%

Stroke Induces Gene Profile Changes Associated with Neurogenesis and Angiogenesis in Adult Subventricular Zone Progenitor Cells

Liu¹,

Zhang²,

Zhang³

et al. 2006

J Cereb Blood Flow Metab

107

100

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Neural progenitor cells in the subventricular zone (SVZ) of the lateral ventricular wall give rise to new neurons throughout rodent life. Ischemic stroke induces angiogenesis and neurogenesis. Using laser capture microdissection (LCM) in combination with microarrays containing approximately 400 known genes associated with stem cells and angiogenesis, we investigated gene profiles of SVZ cells in the adult mouse subjected to middle cerebral artery occlusion. Our data revealed that nonstroke SVZ cells expressed sets of genes that are important for neural progenitor cell proliferation, differentiation, and migration. In addition, stroke SVZ cells expressed many genes involved in neurogenesis during embryonic development but were not detected in nonstroke SVZ cells. Stroke upregulated genes were verified by real-time reverse transcriptase-polymerase chain reaction and immunostaining. These data indicate that adult SVZ cells recapture embryonic molecular signals after stroke and provide insight into the molecular mechanisms, which regulate the biological function of neural progenitor cells in the SVZ of adult rodent brain under physiological and stroke conditions.

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Section: Discussionmentioning

confidence: 99%

Stroke Induces Gene Profile Changes Associated with Neurogenesis and Angiogenesis in Adult Subventricular Zone Progenitor Cells

Liu¹,

Zhang²,

Zhang³

et al. 2006

J Cereb Blood Flow Metab

107

100

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“…RNA microarray technology allows for the mapping of the time course of gene responses and differential expression of thousands of genes in the brain triggered by ischemic insult 9,15,20) . Transient focal cerebral ischemia induces complex changes in the genomic profile, including the expression of new genes and upregulation and downregulation of genes, which occur distinctly in a temporal manner.…”

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confidence: 99%

Changes in Gene Expression in the Rat Hippocampus after Focal Cerebral Ischemia

Chung

Kim

et al. 2011

J Korean Neurosurg Soc

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Objective : The rat middle cerebral artery thread-occlusion model has been widely used to investigate the pathophysiological mechanisms of stroke and to develop therapeutic treatment. This study was conducted to analyze energy metabolism, apoptotic signal pathways, and genetic changes in the hippocampus of the ischemic rat brain. Methods : Focal transient cerebral ischemia was induced by obstructing the middle cerebral artery for two hours. After 24 hours, the induction of ischemia was confirmed by the measurement of infarct size using 2,3,5-triphenyltetrazolium chloride staining. A cDNA microarray assay was performed after isolating the hippocampus, and was used to examine changes in genetic expression patterns. Results : According to the cDNA microarray analysis, a total of 1,882 and 2,237 genes showed more than a 2-fold increase and more than a 2-fold decrease, respectively. When the genes were classified according to signal pathways, genes related with oxidative phosphorylation were found most frequently. There are several apoptotic genes that are known to be expressed during ischemic brain damage, including Akt2 and Tnfrsf1a. In this study, the expression of these genes was observed to increase by more than 2-fold. As energy metabolism related genes grew, ischemic brain damage was affected, and the expression of important genes related to apoptosis was increased/decreased. Conclusion : Our analysis revealed a significant change in the expression of energy metabolism related genes (Atp6v0d1, Atp5g2, etc.) in the hippocampus of the ischemic rat brain. Based on this data, we feel these genes have the potential to be target genes used for the development of therapeutic agents for ischemic stroke.

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“…Several examples of studies that have used microarray analysis of brain homogenates during the past few years to examine gross regional gene expression profiles in rodent models of such complex brain disorders as TBI, stroke, and epilepsy are summarized in Table I, along with the species, conditions, and types of arrays that were used for each comparison. [25][26][27][28][29][30][31][32][33] All five of the TBI studies listed in Table I employed a controlled cortical impact (CCI) model of injury, but different strains and species were used in the different studies. The microarrays most frequently used for all of the rat studies were the Affymetrix U34 Rat Neurobiology array and U34 Rat Genome Set, whereas different arrays were used for each of the mouse studies.…”

Section: Gene Expression Profiling Using Brain Homogenatesmentioning

confidence: 99%

“…28 CCI (male c57/BL6 Cortex (2 h, 6 h, 24 h, 3 days, Incyte GEM 2 cDNA Ipsilateral injured frontal mice, 20 g-27 g) a and 14 days postinjury) microarray chips 6 mm of cortex vs. naive (n ϭ 10 pooled) Matzilevich et al 29 CCI (male Long-Evans Hippocampus (3 h and Affymetrix Rat Genome Ipsilateral injured rats, 250 g-275 g) a 24 h postinjury) U34A GeneChip, aRNA hippocampus vs. sham (T7) amplification (n ϭ 10 were pooled) Rao et al 30 MCAO (male spontaneously Frontoparietal cortex Affymetrix Rat Neurobiology Ipsilateral injured cortex hypertensive rats, 280 g-320 g) b (6 h and 24 h postinfarction) U34 GeneChip vs. contralat. cortex (n ϭ 3 per each of 3 chips per group were pooled) Schmidt-Kastner et al 31 MCAO (male Sprague-Dawly Peri-ischemic cortex Incyte Mouse UniGene 1 Ipsilateral injured cortex vs. rats, 263 g-370 g) b (3 h postinfarction) microarray sham (n ϭ 2 per each of 3 chips per group were pooled) Elliott et al 32 Drug-induced and terminated Dentate gyrus: 14 days after Affymetrix Rat Genome Bilateral dentate gyrus after SE status epilepticus (male status epilepticus (SE) and U34A GeneChip vs. P3 (n ϭ 2 to 3 from adult Sprague-Dawley rats, 180 g-200 g) 3 days postnatal or n ϭ 10 to 12 from P3 animals pooled) Lukasiuk et al 33 Amygdala stimulation with Temporal lobe and hippocampus Research Genetics GF300 Bilateral hippocampus and electrode (male Sprague-Dawley (1 day, 4 days, 1 week, 2 weeks filter cDNA microarrays temporal lobes after SE vs. rats, 290 g-360 g) with seizures and 2 weeks without controls (n ϭ 2 to 3 were seizures after SE) pooled per chip per group) a CCI-Controlled Cortical Impact brain injury. b MCAO-Middle Cerebral Artery Occlusion.…”

Section: Gene Expression Profiling Using Brain Homogenatesmentioning

confidence: 99%

“…21,[34][35][36] Instead, it combines all of the different cell types present in a sample tissue (neurons, glia, blood cells and vessels, and so forth) at potentially disparate stages of injury and disease processes. [25][26][27][28][29][30][31][32][33] As a result, the gene expression profiles of selectively vulnerable subpopulations of cells may be largely obscured, and the detection of potentially important, less abundantly expressed genes (such as transcription factors) may be overlooked. Identification of the source of an observed pattern of differential gene expression can also be more difficult when tissue homogenates are used for gene expression profiling.…”

Section: Single-cell Gene Expression Profilingmentioning

confidence: 99%

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Methodological Considerations Regarding Single-Cell Gene Expression Profiling for Brain Injury

et al. 2004

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Genomic microarrays are rapidly becoming ubiquitous throughout a wide variety of biological disciplines. As their use has grown during the past few years, many important discoveries have been made in the fields of central nervous system (CNS) injury and disease using this emerging technology. In addition, single-cell mRNA amplification techniques are now being used along with microarrays to overcome many of the difficulties associated with the cellular heterogeneity of the brain. This development has extended the utility of gene expression profiling and has provided researchers with exciting new insights into the neuropathology of CNS injury and disease at a molecular and cellular level. New methodological, standardization, and statistical techniques are currently being developed to improve the reproducibility of microarrays and facilitate the analysis of large amounts of data. In this review, we will discuss the application of these techniques to experimental, clinically relevant models of traumatic brain injury.

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DNA microarray analysis of cortical gene expression during early recirculation after focal brain ischemia in rat

Cited by 100 publications

References 76 publications

Stroke Induces Gene Profile Changes Associated with Neurogenesis and Angiogenesis in Adult Subventricular Zone Progenitor Cells

Stroke Induces Gene Profile Changes Associated with Neurogenesis and Angiogenesis in Adult Subventricular Zone Progenitor Cells

Changes in Gene Expression in the Rat Hippocampus after Focal Cerebral Ischemia

Methodological Considerations Regarding Single-Cell Gene Expression Profiling for Brain Injury

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