Adenoviral expression of CREB protects neurons from apoptotic and excitotoxic stress
In this study we have used a molecular approach to manipulate CREB gene expression to study its role in the regulation of neuronal cell death. To achieve this, adenoviral (Ad) vectors encoding EGFP, CREB, and a powerful CREB dominant-negative, known as A-CREB were constructed. The over-expression of...
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Veröffentlicht in: | Neuroreport 2004-05, Vol.15 (7), p.1171-1175 |
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creator | Glover, Colin P. J Heywood, Darren J Bienemann, Alison S Deuschle, Ulrich Kew, James N. C Uney, James B |
description | In this study we have used a molecular approach to manipulate CREB gene expression to study its role in the regulation of neuronal cell death. To achieve this, adenoviral (Ad) vectors encoding EGFP, CREB, and a powerful CREB dominant-negative, known as A-CREB were constructed. The over-expression of CREB but not A-CREB was found to protect primary hippocampal neurons from staurosporine-induced apoptosis, glutamate induced excitotoxicity and exposure to an in vitro ischaemic stress. Hence, manipulating CREB-regulated pathways may provide a means of delaying or preventing the neuronal cell death associated with ischaemic related injury, and in neurodegenerative diseases such as Huntingtonʼs and Alzheimerʼs disease. |
doi_str_mv | 10.1097/00001756-200405190-00018 |
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J ; Heywood, Darren J ; Bienemann, Alison S ; Deuschle, Ulrich ; Kew, James N. C ; Uney, James B</creator><creatorcontrib>Glover, Colin P. J ; Heywood, Darren J ; Bienemann, Alison S ; Deuschle, Ulrich ; Kew, James N. C ; Uney, James B</creatorcontrib><description>In this study we have used a molecular approach to manipulate CREB gene expression to study its role in the regulation of neuronal cell death. To achieve this, adenoviral (Ad) vectors encoding EGFP, CREB, and a powerful CREB dominant-negative, known as A-CREB were constructed. The over-expression of CREB but not A-CREB was found to protect primary hippocampal neurons from staurosporine-induced apoptosis, glutamate induced excitotoxicity and exposure to an in vitro ischaemic stress. Hence, manipulating CREB-regulated pathways may provide a means of delaying or preventing the neuronal cell death associated with ischaemic related injury, and in neurodegenerative diseases such as Huntingtonʼs and Alzheimerʼs disease.</description><identifier>ISSN: 0959-4965</identifier><identifier>EISSN: 1473-558X</identifier><identifier>DOI: 10.1097/00001756-200405190-00018</identifier><identifier>PMID: 15129168</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>Adenoviridae - genetics ; Animals ; Apoptosis - drug effects ; Apoptosis - physiology ; Biological and medical sciences ; Cell Survival - drug effects ; Cell Survival - physiology ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein - biosynthesis ; Cyclic AMP Response Element-Binding Protein - genetics ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Excitatory Amino Acid Agonists - pharmacology ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - physiology ; HeLa Cells ; Hippocampus - drug effects ; Hippocampus - metabolism ; Humans ; Medical sciences ; Neurology ; Neurons - drug effects ; Neurons - metabolism ; Rats ; Rats, Wistar ; Stress, Physiological - genetics ; Stress, Physiological - metabolism ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroreport, 2004-05, Vol.15 (7), p.1171-1175</ispartof><rights>2004 Lippincott Williams & Wilkins, Inc.</rights><rights>2004 INIST-CNRS</rights><rights>Copyright 2004 Lippincott Williams and Wilkins</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4178-b91be7701680d0fe16fe06f2449f878c013e3cc802ff29dd35c4277655b76263</citedby><cites>FETCH-LOGICAL-c4178-b91be7701680d0fe16fe06f2449f878c013e3cc802ff29dd35c4277655b76263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15927123$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15129168$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Glover, Colin P. J</creatorcontrib><creatorcontrib>Heywood, Darren J</creatorcontrib><creatorcontrib>Bienemann, Alison S</creatorcontrib><creatorcontrib>Deuschle, Ulrich</creatorcontrib><creatorcontrib>Kew, James N. C</creatorcontrib><creatorcontrib>Uney, James B</creatorcontrib><title>Adenoviral expression of CREB protects neurons from apoptotic and excitotoxic stress</title><title>Neuroreport</title><addtitle>Neuroreport</addtitle><description>In this study we have used a molecular approach to manipulate CREB gene expression to study its role in the regulation of neuronal cell death. To achieve this, adenoviral (Ad) vectors encoding EGFP, CREB, and a powerful CREB dominant-negative, known as A-CREB were constructed. The over-expression of CREB but not A-CREB was found to protect primary hippocampal neurons from staurosporine-induced apoptosis, glutamate induced excitotoxicity and exposure to an in vitro ischaemic stress. Hence, manipulating CREB-regulated pathways may provide a means of delaying or preventing the neuronal cell death associated with ischaemic related injury, and in neurodegenerative diseases such as Huntingtonʼs and Alzheimerʼs disease.</description><subject>Adenoviridae - genetics</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - physiology</subject><subject>Cells, Cultured</subject><subject>Cyclic AMP Response Element-Binding Protein - biosynthesis</subject><subject>Cyclic AMP Response Element-Binding Protein - genetics</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Excitatory Amino Acid Agonists - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - physiology</subject><subject>HeLa Cells</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Stress, Physiological - genetics</subject><subject>Stress, Physiological - metabolism</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0959-4965</issn><issn>1473-558X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctOxCAUhonR6Hh5BcNGd1WgUGCpE2-JiYmZhTvC0EOsdkqF1svbyzjjZSMbcsj3n3PygRCm5IQSLU9JPlSKqmCEcCKoJsXyRW2gCeWyLIRQD5toQrTQBdeV2EG7KT1lRGdoG-1QQZmmlZqg2VkNXXhtom0xvPcRUmpCh4PH0_uLc9zHMIAbEu5gjKFL2MewwLYP_RCGxmHb1TnmmlyF91ynYdlhH2152yY4WN97aHZ5MZteF7d3VzfTs9vCcSpVMdd0DlKSvAipiQdaeSCVZ5xrr6RyhJZQOqcI857pui6F40zKSoi5rFhV7qHjVdu85csIaTCLJjloW9tBGJNhhGtOlcygWoEuhpQieNPHZmHjh6HELIWab6HmR6j5Epqjh-sZ43wB9W9wbTADR2vAJmdbH23nmvSH00xSVmaOr7i30A4Q03M7vkE0j2Db4dH896HlJ6UujVs</recordid><startdate>20040519</startdate><enddate>20040519</enddate><creator>Glover, Colin P. 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C ; Uney, James B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4178-b91be7701680d0fe16fe06f2449f878c013e3cc802ff29dd35c4277655b76263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adenoviridae - genetics</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - physiology</topic><topic>Cells, Cultured</topic><topic>Cyclic AMP Response Element-Binding Protein - biosynthesis</topic><topic>Cyclic AMP Response Element-Binding Protein - genetics</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Excitatory Amino Acid Agonists - pharmacology</topic><topic>Fundamental and applied biological sciences. 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C</au><au>Uney, James B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adenoviral expression of CREB protects neurons from apoptotic and excitotoxic stress</atitle><jtitle>Neuroreport</jtitle><addtitle>Neuroreport</addtitle><date>2004-05-19</date><risdate>2004</risdate><volume>15</volume><issue>7</issue><spage>1171</spage><epage>1175</epage><pages>1171-1175</pages><issn>0959-4965</issn><eissn>1473-558X</eissn><abstract>In this study we have used a molecular approach to manipulate CREB gene expression to study its role in the regulation of neuronal cell death. To achieve this, adenoviral (Ad) vectors encoding EGFP, CREB, and a powerful CREB dominant-negative, known as A-CREB were constructed. The over-expression of CREB but not A-CREB was found to protect primary hippocampal neurons from staurosporine-induced apoptosis, glutamate induced excitotoxicity and exposure to an in vitro ischaemic stress. Hence, manipulating CREB-regulated pathways may provide a means of delaying or preventing the neuronal cell death associated with ischaemic related injury, and in neurodegenerative diseases such as Huntingtonʼs and Alzheimerʼs disease.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>15129168</pmid><doi>10.1097/00001756-200405190-00018</doi><tpages>5</tpages></addata></record> |
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subjects | Adenoviridae - genetics Animals Apoptosis - drug effects Apoptosis - physiology Biological and medical sciences Cell Survival - drug effects Cell Survival - physiology Cells, Cultured Cyclic AMP Response Element-Binding Protein - biosynthesis Cyclic AMP Response Element-Binding Protein - genetics Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Excitatory Amino Acid Agonists - pharmacology Fundamental and applied biological sciences. Psychology Gene Expression Regulation - drug effects Gene Expression Regulation - physiology HeLa Cells Hippocampus - drug effects Hippocampus - metabolism Humans Medical sciences Neurology Neurons - drug effects Neurons - metabolism Rats Rats, Wistar Stress, Physiological - genetics Stress, Physiological - metabolism Vertebrates: nervous system and sense organs |
title | Adenoviral expression of CREB protects neurons from apoptotic and excitotoxic stress |
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