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

2011 ◽  
Vol 50 (3) ◽  
pp. 173 ◽  
Author(s):  
Jun Young Chung ◽  
Jae Woo Yi ◽  
Sung Min Kim ◽  
Young Jin Lim ◽  
Joo Ho Chung ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Rat Hippocampus

Gene expression profiling of the rat hippocampus one month after focal cerebral ischemia followed by enriched environment

2005 ◽  
Vol 385 (2) ◽  
pp. 173-178 ◽  
Author(s):  
Annica Rönnbäck ◽  
Per Dahlqvist ◽  
Per-Arne Svensson ◽  
Margareta Jernås ◽  
Björn Carlsson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cerebral Ischemia ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Focal Cerebral Ischemia ◽  
Enriched Environment ◽  
Rat Hippocampus

scholarly journals Temporal Gene Expression Profiles after Focal Cerebral Ischemia in Mice

2018 ◽  
Vol 9 (2) ◽  
pp. 249 ◽  
Author(s):  
Chengjie Zhang ◽  
Yanbing Zhu ◽  
Song Wang ◽  
Zheng Zachory Wei ◽  
Michael Qize Jiang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Temporal Gene Expression

scholarly journals Serial Analysis of Gene Expression Identifies Metallothionein-II as Major Neuroprotective Gene in Mouse Focal Cerebral Ischemia

2002 ◽  
Vol 22 (14) ◽  
pp. 5879-5888 ◽  
Author(s):  
George Trendelenburg ◽  
Konstantin Prass ◽  
Josef Priller ◽  
Krisztian Kapinya ◽  
Andreas Polley ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia

scholarly journals Restriction-mediated Differential Display (RMDD) Identifies pip92 as a Pro-Apoptotic Gene Product Induced during Focal Cerebral Ischemia

2004 ◽  
Vol 24 (2) ◽  
pp. 224-236 ◽  
Author(s):  
Armin Schneider ◽  
Achim Fischer ◽  
Daniela Weber ◽  
Oliver von Ahsen ◽  
Sigrid Scheek ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cerebral Ischemia ◽  
Differential Display ◽  
Focal Cerebral Ischemia ◽  
Screening Method ◽  
Artery Occlusion ◽  
Selection Strategy ◽  
Complex Samples ◽  
Apoptotic Activity ◽  
Cerebral Artery Occlusion

Studies of gene expression changes after cerebral ischemia can provide novel insight into ischemic pathophysiology. Here we describe application of restriction-mediated differential display to screening for differentially expressed genes after focal cerebral ischemia. This method combines the nonredundant generation of biotin-labeled fragment sets with the excellent resolution of direct blotting electrophoresis, reliable fragment recovery, and a novel clone selection strategy. Using the filament model in mouse with 90 minutes MCA occlusion followed by 2, 6, and 20 hours reperfusion, we have compared gene expression in sham-operated animals to both the ipsi- and contralateral forebrain hemisphere of ischemic mice. Our screening method has resulted in the identification of 70 genes differentially regulated after transient middle cerebral artery occlusion (MCAO), several of which represent unknown clones. We have identified many of the previously published regulated genes, lending high credibility to our method. Surprisingly, we detected a high degree of correspondent regulation of genes in the nonischemic hemisphere. A high percentage of genes coding for proteins in the respiratory chain was found to be up-regulated after ischemia, potentially representing a new mechanism involved in counteracting energy failure or radical generation in cerebral ischemia. One particularly interesting gene, whose upregulation by ischemia has not been described before, is pip92; this gene shows a rapid and long-lasting induction after cerebral ischemia. Here we demonstrate that pip92 induces cell death in primary neurons and displays several hallmarks of pro-apoptotic activity upon overexpression, supporting the notion that we have identified a novel pathophysiological player in cerebral ischemia. In summary, restriction-mediated differential display has proven its suitability for screening complex samples such as brain to reliably identify regulated genes, which can uncover novel pathophysiological mechanisms.

Transforming growth factor-β1 exhibits delayed gene expression following focal cerebral ischemia

1995 ◽  
Vol 36 (6) ◽  
pp. 607-609 ◽  
Author(s):  
Xinkang Wang ◽  
Tian-Li Yue ◽  
Raymond F. White ◽  
Frank C. Barone ◽  
Giora Z. Feuerstein
Keyword(s):  
Gene Expression ◽  
Cerebral Ischemia ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Focal Cerebral Ischemia ◽  
Transforming Growth Factor Β1

scholarly journals Brief Focal Cerebral Ischemia That Simulates Transient Ischemic Attacks in Humans Regulates Gene Expression in Rat Peripheral Blood

2009 ◽  
Vol 30 (1) ◽  
pp. 110-118 ◽  
Author(s):  
Xinhua Zhan ◽  
Bradley P Ander ◽  
Glen Jickling ◽  
Renée Turner ◽  
Boryana Stamova ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Peripheral Blood ◽  
Focal Cerebral Ischemia ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Focal Ischemia ◽  
Transient Ischemic Attacks

Blood gene expression profiles of very brief (5 and 10 mins) focal ischemia that simulates transient ischemic attacks in humans were compared with ischemic stroke (120 mins focal ischemia), sham, and naïve controls. The number of significantly regulated genes after 5 and 10 mins of cerebral ischemia was 39 and 160, respectively (fold change ⩾∣1.5∣ and P<0.05). There were 103 genes common to brief focal ischemia and ischemic stroke. Ingenuity pathway analysis showed that genes regulated in the 5 mins group were mainly involved in small molecule biochemistry. Genes regulated in the 10 mins group were involved in cell death, development, growth, and proliferation. Such genes were also regulated in the ischemic stroke group. Genes common to ischemia were involved in the inflammatory response, immune response, and cell death—indicating that these pathways are a feature of focal ischemia, regardless of the duration. These results provide evidence that brief focal ischemia differentially regulates gene expression in the peripheral blood in a manner that could distinguish brief focal ischemia from ischemic stroke and controls in rats. We postulate that this will also occur in humans.

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