Transcriptional response to circumscribed cortical brain ischemia: spatiotemporal patterns in ischemic vs. remote non-ischemic cortex
Focal brain infarcts are surrounded by extended perilesional zones that comprise the partially ischemic penumbra but also completely non‐ischemic cortex of the remote ipsilateral hemisphere. To delineate the impact of lesion‐associated vs. remote processes on transcriptional programming after focal...
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| Veröffentlicht in: | The European journal of neuroscience 2004-04, Vol.19 (7), p.1708-1720 |
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| description | Focal brain infarcts are surrounded by extended perilesional zones that comprise the partially ischemic penumbra but also completely non‐ischemic cortex of the remote ipsilateral hemisphere. To delineate the impact of lesion‐associated vs. remote processes on transcriptional programming after focal ischemia, we used cDNA array analysis, quantitative real‐time polymerase chain reaction and immunohistochemistry in the photothrombosis model of circumscribed cortical ischemia in rats. At an early stage of 4 h after ischemia, gene induction occurred to a similar extent in the ischemic infarct and remote non‐ischemic cortex of the ipsilateral hemisphere. Among the genes induced in non‐ischemic cortex we found the NGF‐inducible genes PC3, VGF and Arc, the transcriptional regulators IκB‐α and Stat3, and the β‐chemokine MIP‐1α (CCL3). At 3 days, the spatial pattern of gene expression had changed dramatically with brain fatty acid‐binding protein as the only gene significantly induced in non‐ischemic ipsilateral cortex. In contrast, numerous genes were exclusively regulated at the lesion site, comprising genes involved in cell cycle regulation, proteolysis, apoptosis, lipid homeostasis and anti‐inflammatory counter‐regulation. Cortical spreading depression was identified as the main mechanism underlying gene induction in remote non‐ischemic cortex. Our data demonstrate a dynamic spatiotemporal pattern of gene induction, which may contribute to delayed progression of damage or, alternatively, mediate neuroprotection, tissue remodeling and functional compensation. |
| doi_str_mv | 10.1111/j.1460-9568.2004.03226.x |
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To delineate the impact of lesion‐associated vs. remote processes on transcriptional programming after focal ischemia, we used cDNA array analysis, quantitative real‐time polymerase chain reaction and immunohistochemistry in the photothrombosis model of circumscribed cortical ischemia in rats. At an early stage of 4 h after ischemia, gene induction occurred to a similar extent in the ischemic infarct and remote non‐ischemic cortex of the ipsilateral hemisphere. Among the genes induced in non‐ischemic cortex we found the NGF‐inducible genes PC3, VGF and Arc, the transcriptional regulators IκB‐α and Stat3, and the β‐chemokine MIP‐1α (CCL3). At 3 days, the spatial pattern of gene expression had changed dramatically with brain fatty acid‐binding protein as the only gene significantly induced in non‐ischemic ipsilateral cortex. In contrast, numerous genes were exclusively regulated at the lesion site, comprising genes involved in cell cycle regulation, proteolysis, apoptosis, lipid homeostasis and anti‐inflammatory counter‐regulation. Cortical spreading depression was identified as the main mechanism underlying gene induction in remote non‐ischemic cortex. Our data demonstrate a dynamic spatiotemporal pattern of gene induction, which may contribute to delayed progression of damage or, alternatively, mediate neuroprotection, tissue remodeling and functional compensation.</description><identifier>ISSN: 0953-816X</identifier><identifier>EISSN: 1460-9568</identifier><identifier>DOI: 10.1111/j.1460-9568.2004.03226.x</identifier><identifier>PMID: 15078545</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science, Ltd</publisher><subject>AIDS-Related Complex - genetics ; AIDS-Related Complex - metabolism ; Animals ; Brain Ischemia - complications ; Brain Ischemia - genetics ; Carrier Proteins - genetics ; Carrier Proteins - metabolism ; Cathepsin K ; Cathepsins - genetics ; Cathepsins - metabolism ; Cdc20 Proteins ; Cell Cycle Proteins - genetics ; Cell Cycle Proteins - metabolism ; Cerebral Cortex - metabolism ; Cerebral Cortex - pathology ; Cerebral Cortex - physiopathology ; Cerebral Infarction - etiology ; Cerebral Infarction - genetics ; cortical spreading depression ; Cortical Spreading Depression - drug effects ; Dizocilpine Maleate - pharmacology ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Drug Interactions ; Excitatory Amino Acid Antagonists - pharmacology ; Fatty Acid-Binding Protein 7 ; Fatty Acid-Binding Proteins ; Functional Laterality - genetics ; Functional Laterality - physiology ; gene expression profiling ; Gene Expression Profiling - methods ; Gene Expression Regulation - drug effects ; HSP70 Heat-Shock Proteins - genetics ; HSP70 Heat-Shock Proteins - metabolism ; Immunohistochemistry - methods ; Male ; Nerve Tissue Proteins ; neuroprotection ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Oligonucleotide Array Sequence Analysis - methods ; Phosphoric Monoester Hydrolases - genetics ; Phosphoric Monoester Hydrolases - metabolism ; plasticity ; Potassium Chloride - pharmacology ; Proprotein Convertase 1 - genetics ; Proprotein Convertase 1 - metabolism ; rat ; Rats ; Rats, Wistar ; Receptors, Cytoplasmic and Nuclear ; Receptors, Steroid ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - biosynthesis ; STAT3 Transcription Factor ; Time Factors ; Trans-Activators - metabolism ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Transcription, Genetic ; Transcriptional Activation</subject><ispartof>The European journal of neuroscience, 2004-04, Vol.19 (7), p.1708-1720</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4656-698721fd501cf05f37283dc0e5a19a813f6f1e7161ac42f05cca70dfe2eebb793</citedby><cites>FETCH-LOGICAL-c4656-698721fd501cf05f37283dc0e5a19a813f6f1e7161ac42f05cca70dfe2eebb793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1460-9568.2004.03226.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1460-9568.2004.03226.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15078545$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Küry, Patrick</creatorcontrib><creatorcontrib>Schroeter, Michael</creatorcontrib><creatorcontrib>Jander, Sebastian</creatorcontrib><title>Transcriptional response to circumscribed cortical brain ischemia: spatiotemporal patterns in ischemic vs. remote non-ischemic cortex</title><title>The European journal of neuroscience</title><addtitle>Eur J Neurosci</addtitle><description>Focal brain infarcts are surrounded by extended perilesional zones that comprise the partially ischemic penumbra but also completely non‐ischemic cortex of the remote ipsilateral hemisphere. To delineate the impact of lesion‐associated vs. remote processes on transcriptional programming after focal ischemia, we used cDNA array analysis, quantitative real‐time polymerase chain reaction and immunohistochemistry in the photothrombosis model of circumscribed cortical ischemia in rats. At an early stage of 4 h after ischemia, gene induction occurred to a similar extent in the ischemic infarct and remote non‐ischemic cortex of the ipsilateral hemisphere. Among the genes induced in non‐ischemic cortex we found the NGF‐inducible genes PC3, VGF and Arc, the transcriptional regulators IκB‐α and Stat3, and the β‐chemokine MIP‐1α (CCL3). At 3 days, the spatial pattern of gene expression had changed dramatically with brain fatty acid‐binding protein as the only gene significantly induced in non‐ischemic ipsilateral cortex. In contrast, numerous genes were exclusively regulated at the lesion site, comprising genes involved in cell cycle regulation, proteolysis, apoptosis, lipid homeostasis and anti‐inflammatory counter‐regulation. Cortical spreading depression was identified as the main mechanism underlying gene induction in remote non‐ischemic cortex. Our data demonstrate a dynamic spatiotemporal pattern of gene induction, which may contribute to delayed progression of damage or, alternatively, mediate neuroprotection, tissue remodeling and functional compensation.</description><subject>AIDS-Related Complex - genetics</subject><subject>AIDS-Related Complex - metabolism</subject><subject>Animals</subject><subject>Brain Ischemia - complications</subject><subject>Brain Ischemia - genetics</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - metabolism</subject><subject>Cathepsin K</subject><subject>Cathepsins - genetics</subject><subject>Cathepsins - metabolism</subject><subject>Cdc20 Proteins</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - pathology</subject><subject>Cerebral Cortex - physiopathology</subject><subject>Cerebral Infarction - etiology</subject><subject>Cerebral Infarction - genetics</subject><subject>cortical spreading depression</subject><subject>Cortical Spreading Depression - drug effects</subject><subject>Dizocilpine Maleate - pharmacology</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Drug Interactions</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Fatty Acid-Binding Protein 7</subject><subject>Fatty Acid-Binding Proteins</subject><subject>Functional Laterality - genetics</subject><subject>Functional Laterality - physiology</subject><subject>gene expression profiling</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation - drug effects</subject><subject>HSP70 Heat-Shock Proteins - genetics</subject><subject>HSP70 Heat-Shock Proteins - metabolism</subject><subject>Immunohistochemistry - methods</subject><subject>Male</subject><subject>Nerve Tissue Proteins</subject><subject>neuroprotection</subject><subject>Nuclear Receptor Subfamily 4, Group A, Member 1</subject><subject>Oligonucleotide Array Sequence Analysis - methods</subject><subject>Phosphoric Monoester Hydrolases - genetics</subject><subject>Phosphoric Monoester Hydrolases - metabolism</subject><subject>plasticity</subject><subject>Potassium Chloride - pharmacology</subject><subject>Proprotein Convertase 1 - genetics</subject><subject>Proprotein Convertase 1 - metabolism</subject><subject>rat</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Cytoplasmic and Nuclear</subject><subject>Receptors, Steroid</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - biosynthesis</subject><subject>STAT3 Transcription Factor</subject><subject>Time Factors</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Transcription, Genetic</subject><subject>Transcriptional Activation</subject><issn>0953-816X</issn><issn>1460-9568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkctu3CAUhlHVqJmkeYWIVXd2wDYXV-qiinLVaLLI5LJDGB8rTG3jgqedPEDeuzgzmmzLBg7n-3_QfxDClKQ0rrNVSgtOkpJxmWaEFCnJs4ynm09otm98RjNSsjyRlD8foqMQVoQQyQv2BR1SRoRkBZuht6XXfTDeDqN1vW6xhzC4PgAeHTbWm3U3dSuosXF-tCYilde2xzaYF-is_o7DoKN4hG5wPrZjNYLvA_6ADP4T0mjdRQr3rk_295MpbL6ig0a3AU52-zF6uLxYnl8n87urm_Of88QUnPGEl1JktKkZoaYhrMlFJvPaEGCallrSvOENBUE51abIImGMFqRuIAOoKlHmx-jb1nfw7vcawqi6-BNoW92DWwdFhRBSFFkE5RY03oXgoVGDt532r4oSNY1ArdSUtJqSVtMI1PsI1CZKT3dvrKsO6g_hLvMI_NgCf20Lr_9trC5uF9Mp6pOt3oYY3V6v_S_FRS6Yelpcqfvrx0u-nIr8Hy1-qDI</recordid><startdate>200404</startdate><enddate>200404</enddate><creator>Küry, Patrick</creator><creator>Schroeter, Michael</creator><creator>Jander, Sebastian</creator><general>Blackwell Science, Ltd</general><scope>BSCLL</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></search><sort><creationdate>200404</creationdate><title>Transcriptional response to circumscribed cortical brain ischemia: spatiotemporal patterns in ischemic vs. remote non-ischemic cortex</title><author>Küry, Patrick ; Schroeter, Michael ; Jander, Sebastian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4656-698721fd501cf05f37283dc0e5a19a813f6f1e7161ac42f05cca70dfe2eebb793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>AIDS-Related Complex - genetics</topic><topic>AIDS-Related Complex - metabolism</topic><topic>Animals</topic><topic>Brain Ischemia - complications</topic><topic>Brain Ischemia - genetics</topic><topic>Carrier Proteins - genetics</topic><topic>Carrier Proteins - metabolism</topic><topic>Cathepsin K</topic><topic>Cathepsins - genetics</topic><topic>Cathepsins - metabolism</topic><topic>Cdc20 Proteins</topic><topic>Cell Cycle Proteins - genetics</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cerebral Cortex - pathology</topic><topic>Cerebral Cortex - physiopathology</topic><topic>Cerebral Infarction - etiology</topic><topic>Cerebral Infarction - genetics</topic><topic>cortical spreading depression</topic><topic>Cortical Spreading Depression - drug effects</topic><topic>Dizocilpine Maleate - pharmacology</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Drug Interactions</topic><topic>Excitatory Amino Acid Antagonists - pharmacology</topic><topic>Fatty Acid-Binding Protein 7</topic><topic>Fatty Acid-Binding Proteins</topic><topic>Functional Laterality - genetics</topic><topic>Functional Laterality - physiology</topic><topic>gene expression profiling</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation - drug effects</topic><topic>HSP70 Heat-Shock Proteins - genetics</topic><topic>HSP70 Heat-Shock Proteins - metabolism</topic><topic>Immunohistochemistry - methods</topic><topic>Male</topic><topic>Nerve Tissue Proteins</topic><topic>neuroprotection</topic><topic>Nuclear Receptor Subfamily 4, Group A, Member 1</topic><topic>Oligonucleotide Array Sequence Analysis - methods</topic><topic>Phosphoric Monoester Hydrolases - genetics</topic><topic>Phosphoric Monoester Hydrolases - metabolism</topic><topic>plasticity</topic><topic>Potassium Chloride - pharmacology</topic><topic>Proprotein Convertase 1 - genetics</topic><topic>Proprotein Convertase 1 - metabolism</topic><topic>rat</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Cytoplasmic and Nuclear</topic><topic>Receptors, Steroid</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA, Messenger - biosynthesis</topic><topic>STAT3 Transcription Factor</topic><topic>Time Factors</topic><topic>Trans-Activators - metabolism</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Transcription, Genetic</topic><topic>Transcriptional Activation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Küry, Patrick</creatorcontrib><creatorcontrib>Schroeter, Michael</creatorcontrib><creatorcontrib>Jander, Sebastian</creatorcontrib><collection>Istex</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><jtitle>The European journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Küry, Patrick</au><au>Schroeter, Michael</au><au>Jander, Sebastian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transcriptional response to circumscribed cortical brain ischemia: spatiotemporal patterns in ischemic vs. remote non-ischemic cortex</atitle><jtitle>The European journal of neuroscience</jtitle><addtitle>Eur J Neurosci</addtitle><date>2004-04</date><risdate>2004</risdate><volume>19</volume><issue>7</issue><spage>1708</spage><epage>1720</epage><pages>1708-1720</pages><issn>0953-816X</issn><eissn>1460-9568</eissn><abstract>Focal brain infarcts are surrounded by extended perilesional zones that comprise the partially ischemic penumbra but also completely non‐ischemic cortex of the remote ipsilateral hemisphere. To delineate the impact of lesion‐associated vs. remote processes on transcriptional programming after focal ischemia, we used cDNA array analysis, quantitative real‐time polymerase chain reaction and immunohistochemistry in the photothrombosis model of circumscribed cortical ischemia in rats. At an early stage of 4 h after ischemia, gene induction occurred to a similar extent in the ischemic infarct and remote non‐ischemic cortex of the ipsilateral hemisphere. Among the genes induced in non‐ischemic cortex we found the NGF‐inducible genes PC3, VGF and Arc, the transcriptional regulators IκB‐α and Stat3, and the β‐chemokine MIP‐1α (CCL3). At 3 days, the spatial pattern of gene expression had changed dramatically with brain fatty acid‐binding protein as the only gene significantly induced in non‐ischemic ipsilateral cortex. In contrast, numerous genes were exclusively regulated at the lesion site, comprising genes involved in cell cycle regulation, proteolysis, apoptosis, lipid homeostasis and anti‐inflammatory counter‐regulation. Cortical spreading depression was identified as the main mechanism underlying gene induction in remote non‐ischemic cortex. Our data demonstrate a dynamic spatiotemporal pattern of gene induction, which may contribute to delayed progression of damage or, alternatively, mediate neuroprotection, tissue remodeling and functional compensation.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science, Ltd</pub><pmid>15078545</pmid><doi>10.1111/j.1460-9568.2004.03226.x</doi><tpages>13</tpages></addata></record> |
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| ispartof | The European journal of neuroscience, 2004-04, Vol.19 (7), p.1708-1720 |
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| subjects | AIDS-Related Complex - genetics AIDS-Related Complex - metabolism Animals Brain Ischemia - complications Brain Ischemia - genetics Carrier Proteins - genetics Carrier Proteins - metabolism Cathepsin K Cathepsins - genetics Cathepsins - metabolism Cdc20 Proteins Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Cerebral Cortex - metabolism Cerebral Cortex - pathology Cerebral Cortex - physiopathology Cerebral Infarction - etiology Cerebral Infarction - genetics cortical spreading depression Cortical Spreading Depression - drug effects Dizocilpine Maleate - pharmacology DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Drug Interactions Excitatory Amino Acid Antagonists - pharmacology Fatty Acid-Binding Protein 7 Fatty Acid-Binding Proteins Functional Laterality - genetics Functional Laterality - physiology gene expression profiling Gene Expression Profiling - methods Gene Expression Regulation - drug effects HSP70 Heat-Shock Proteins - genetics HSP70 Heat-Shock Proteins - metabolism Immunohistochemistry - methods Male Nerve Tissue Proteins neuroprotection Nuclear Receptor Subfamily 4, Group A, Member 1 Oligonucleotide Array Sequence Analysis - methods Phosphoric Monoester Hydrolases - genetics Phosphoric Monoester Hydrolases - metabolism plasticity Potassium Chloride - pharmacology Proprotein Convertase 1 - genetics Proprotein Convertase 1 - metabolism rat Rats Rats, Wistar Receptors, Cytoplasmic and Nuclear Receptors, Steroid Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - biosynthesis STAT3 Transcription Factor Time Factors Trans-Activators - metabolism Transcription Factors - genetics Transcription Factors - metabolism Transcription, Genetic Transcriptional Activation |
| title | Transcriptional response to circumscribed cortical brain ischemia: spatiotemporal patterns in ischemic vs. remote non-ischemic cortex |
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