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 |
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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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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.</description><identifier>ISSN: 0169-328X</identifier><identifier>EISSN: 1872-6941</identifier><identifier>DOI: 10.1016/S0169-328X(02)00135-3</identifier><identifier>PMID: 12007827</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>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</subject><ispartof>Brain research. Molecular brain research., 2002-05, Vol.101 (1), p.12-22</ispartof><rights>2002 Elsevier Science B.V.</rights><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c542t-bcc2269f7ddbafed8a5136ef30fa93b6cf3b74df6f4c93f1897e940a3deb8d903</citedby><cites>FETCH-LOGICAL-c542t-bcc2269f7ddbafed8a5136ef30fa93b6cf3b74df6f4c93f1897e940a3deb8d903</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13669103$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12007827$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><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><title>Identification of differentially expressed genes induced by transient ischemic stroke</title><title>Brain research. 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. This suggests that LOX-1 may serve a novel function in the brain.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>BIS protein</subject><subject>Brain Ischemia - genetics</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - physiopathology</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - pathology</subject><subject>Cerebral Cortex - physiopathology</subject><subject>Cerebral Infarction - genetics</subject><subject>Cerebral Infarction - metabolism</subject><subject>Cerebral Infarction - physiopathology</subject><subject>Cyr61 protein</subject><subject>DNA, Complementary - analysis</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Gene Expression Regulation - physiology</subject><subject>LOX-1</subject><subject>LOX-1 gene</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle cerebral artery occlusion</subject><subject>Narp protein</subject><subject>Neostriatum - metabolism</subject><subject>Neostriatum - pathology</subject><subject>Neostriatum - physiopathology</subject><subject>Neuroglia - metabolism</subject><subject>Neurology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, LDL - genetics</subject><subject>Receptors, Oxidized LDL</subject><subject>Reperfusion Injury - genetics</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - physiopathology</subject><subject>RNA, Messenger - metabolism</subject><subject>Scavenger Receptors, Class E</subject><subject>Stroke</subject><subject>Stroke - genetics</subject><subject>Stroke - metabolism</subject><subject>Stroke - physiopathology</subject><subject>Subtraction</subject><subject>Up-Regulation - physiology</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0169-328X</issn><issn>1872-6941</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LxDAQhoMouq7-BKUXRQ_VfLRpchJZ_ALBgwreQppMNNpt16Qr7r83-4F73MsME56ZvDwIHRF8QTDhl8-pyJxR8XaG6TnGhJU520IDIiqac1mQbTT4R_bQfoyfOFGCkF20RyjGlaDVAL0-WGh777zRve_arHOZ9c5BmL_qppll8DsJECPY7B1aiJlv7dSkqZ5lfdBt9InMfDQfMPYmi33ovuAA7TjdRDhc9SF6vb15Gd3nj093D6Prx9yUBe3z2hhKuXSVtbV2YIUuCePgGHZaspobx-qqsI67wkjmiJAVyAJrZqEWVmI2RKfLu5PQfU8h9mqckkDT6Ba6aVQV4YLTstoIEsEwLzBLYLkETehiDODUJPixDjNFsJqLVwvxam5VYaoW4tV873j1wbQeg11vrUwn4GQF6Gh045I64-OaY5xLsghwteQgefvxEFQ0SXEy7gOYXtnOb4jyB5tDofY</recordid><startdate>20020530</startdate><enddate>20020530</enddate><creator>Schwarz, David A</creator><creator>Barry, Guy</creator><creator>Mackay, Kenneth B</creator><creator>Manu, Frank</creator><creator>Naeve, Gregory S</creator><creator>Vana, Alicia M</creator><creator>Verge, Gail</creator><creator>Conlon, Paul J</creator><creator>Foster, Alan C</creator><creator>Maki, Richard A</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20020530</creationdate><title>Identification of differentially expressed genes induced by transient ischemic stroke</title><author>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</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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