Identification of differentially expressed genes induced by transient ischemic stroke

We have used a rat model of focal cerebral ischemia to investigate changes in gene expression that occur during stroke. To monitor these changes, we employed representational difference analysis–polymerase chain reaction (PCR). A total of 128 unique gene fragments were isolated, and we selected 13 o...

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Veröffentlicht in:Brain research. Molecular brain research. 2002-05, Vol.101 (1), p.12-22
Hauptverfasser: Schwarz, David A, Barry, Guy, Mackay, Kenneth B, Manu, Frank, Naeve, Gregory S, Vana, Alicia M, Verge, Gail, Conlon, Paul J, Foster, Alan C, Maki, Richard A
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container_issue 1
container_start_page 12
container_title Brain research. Molecular brain research.
container_volume 101
creator Schwarz, David A
Barry, Guy
Mackay, Kenneth B
Manu, Frank
Naeve, Gregory S
Vana, Alicia M
Verge, Gail
Conlon, Paul J
Foster, Alan C
Maki, Richard A
description We have used a rat model of focal cerebral ischemia to investigate changes in gene expression that occur during stroke. To monitor these changes, we employed representational difference analysis–polymerase chain reaction (PCR). A total of 128 unique gene fragments were isolated, and we selected 13 of these for quantitative reverse transcriptase-PCR analysis. Of these 13 genes, we found seven that were differentially expressed. Four of these genes have not previously been implicated in stroke, and include neuronal activity regulated pentraxin (Narp), cystein rich protein 61 (Cyr61), Bcl-2 binding protein BIS (Bcl-2-interacting death suppressor), and lectin-like ox-LDL receptor (LOX-1). We demonstrated differential expression of each gene by quantitative PCR analysis, and in the case of LOX-1, we further confirmed differential expression by in situ hybridization. LOX-1 expression is induced greater than ten fold at the core lesion site, and is essentially localized to the ipsilateral half of the brain. LOX-1 appears to be expressed in a non-neuronal cell type, and it does not appear to be expressed in vascular endothelial cells within the brain. This suggests that LOX-1 may serve a novel function in the brain.
doi_str_mv 10.1016/S0169-328X(02)00135-3
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Molecular brain research.</title><addtitle>Brain Res Mol Brain Res</addtitle><description>We have used a rat model of focal cerebral ischemia to investigate changes in gene expression that occur during stroke. To monitor these changes, we employed representational difference analysis–polymerase chain reaction (PCR). A total of 128 unique gene fragments were isolated, and we selected 13 of these for quantitative reverse transcriptase-PCR analysis. Of these 13 genes, we found seven that were differentially expressed. Four of these genes have not previously been implicated in stroke, and include neuronal activity regulated pentraxin (Narp), cystein rich protein 61 (Cyr61), Bcl-2 binding protein BIS (Bcl-2-interacting death suppressor), and lectin-like ox-LDL receptor (LOX-1). We demonstrated differential expression of each gene by quantitative PCR analysis, and in the case of LOX-1, we further confirmed differential expression by in situ hybridization. LOX-1 expression is induced greater than ten fold at the core lesion site, and is essentially localized to the ipsilateral half of the brain. LOX-1 appears to be expressed in a non-neuronal cell type, and it does not appear to be expressed in vascular endothelial cells within the brain. 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Barry, Guy ; Mackay, Kenneth B ; Manu, Frank ; Naeve, Gregory S ; Vana, Alicia M ; Verge, Gail ; Conlon, Paul J ; Foster, Alan C ; Maki, Richard A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c542t-bcc2269f7ddbafed8a5136ef30fa93b6cf3b74df6f4c93f1897e940a3deb8d903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>BIS protein</topic><topic>Brain Ischemia - genetics</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - physiopathology</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cerebral Cortex - pathology</topic><topic>Cerebral Cortex - physiopathology</topic><topic>Cerebral Infarction - genetics</topic><topic>Cerebral Infarction - metabolism</topic><topic>Cerebral Infarction - physiopathology</topic><topic>Cyr61 protein</topic><topic>DNA, Complementary - analysis</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Gene Expression Regulation - physiology</topic><topic>LOX-1</topic><topic>LOX-1 gene</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle cerebral artery occlusion</topic><topic>Narp protein</topic><topic>Neostriatum - metabolism</topic><topic>Neostriatum - pathology</topic><topic>Neostriatum - physiopathology</topic><topic>Neuroglia - metabolism</topic><topic>Neurology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, LDL - genetics</topic><topic>Receptors, Oxidized LDL</topic><topic>Reperfusion Injury - genetics</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - physiopathology</topic><topic>RNA, Messenger - metabolism</topic><topic>Scavenger Receptors, Class E</topic><topic>Stroke</topic><topic>Stroke - genetics</topic><topic>Stroke - metabolism</topic><topic>Stroke - physiopathology</topic><topic>Subtraction</topic><topic>Up-Regulation - physiology</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schwarz, David A</creatorcontrib><creatorcontrib>Barry, Guy</creatorcontrib><creatorcontrib>Mackay, Kenneth B</creatorcontrib><creatorcontrib>Manu, Frank</creatorcontrib><creatorcontrib>Naeve, Gregory S</creatorcontrib><creatorcontrib>Vana, Alicia M</creatorcontrib><creatorcontrib>Verge, Gail</creatorcontrib><creatorcontrib>Conlon, Paul J</creatorcontrib><creatorcontrib>Foster, Alan C</creatorcontrib><creatorcontrib>Maki, Richard A</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research. Molecular brain research.</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schwarz, David A</au><au>Barry, Guy</au><au>Mackay, Kenneth B</au><au>Manu, Frank</au><au>Naeve, Gregory S</au><au>Vana, Alicia M</au><au>Verge, Gail</au><au>Conlon, Paul J</au><au>Foster, Alan C</au><au>Maki, Richard A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification of differentially expressed genes induced by transient ischemic stroke</atitle><jtitle>Brain research. Molecular brain research.</jtitle><addtitle>Brain Res Mol Brain Res</addtitle><date>2002-05-30</date><risdate>2002</risdate><volume>101</volume><issue>1</issue><spage>12</spage><epage>22</epage><pages>12-22</pages><issn>0169-328X</issn><eissn>1872-6941</eissn><abstract>We have used a rat model of focal cerebral ischemia to investigate changes in gene expression that occur during stroke. To monitor these changes, we employed representational difference analysis–polymerase chain reaction (PCR). A total of 128 unique gene fragments were isolated, and we selected 13 of these for quantitative reverse transcriptase-PCR analysis. Of these 13 genes, we found seven that were differentially expressed. Four of these genes have not previously been implicated in stroke, and include neuronal activity regulated pentraxin (Narp), cystein rich protein 61 (Cyr61), Bcl-2 binding protein BIS (Bcl-2-interacting death suppressor), and lectin-like ox-LDL receptor (LOX-1). We demonstrated differential expression of each gene by quantitative PCR analysis, and in the case of LOX-1, we further confirmed differential expression by in situ hybridization. LOX-1 expression is induced greater than ten fold at the core lesion site, and is essentially localized to the ipsilateral half of the brain. LOX-1 appears to be expressed in a non-neuronal cell type, and it does not appear to be expressed in vascular endothelial cells within the brain. This suggests that LOX-1 may serve a novel function in the brain.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>12007827</pmid><doi>10.1016/S0169-328X(02)00135-3</doi><tpages>11</tpages></addata></record>
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subjects Animals
Biological and medical sciences
BIS protein
Brain Ischemia - genetics
Brain Ischemia - metabolism
Brain Ischemia - physiopathology
Cerebral Cortex - metabolism
Cerebral Cortex - pathology
Cerebral Cortex - physiopathology
Cerebral Infarction - genetics
Cerebral Infarction - metabolism
Cerebral Infarction - physiopathology
Cyr61 protein
DNA, Complementary - analysis
Endothelium, Vascular - metabolism
Gene Expression Regulation - physiology
LOX-1
LOX-1 gene
Male
Medical sciences
Middle cerebral artery occlusion
Narp protein
Neostriatum - metabolism
Neostriatum - pathology
Neostriatum - physiopathology
Neuroglia - metabolism
Neurology
Rats
Rats, Sprague-Dawley
Receptors, LDL - genetics
Receptors, Oxidized LDL
Reperfusion Injury - genetics
Reperfusion Injury - metabolism
Reperfusion Injury - physiopathology
RNA, Messenger - metabolism
Scavenger Receptors, Class E
Stroke
Stroke - genetics
Stroke - metabolism
Stroke - physiopathology
Subtraction
Up-Regulation - physiology
Vascular diseases and vascular malformations of the nervous system
title Identification of differentially expressed genes induced by transient ischemic stroke
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