Identification of ischemic regions in a rat model of stroke
Investigations following stroke first of all require information about the spatio-temporal dimension of the ischemic core as well as of perilesional and remote affected tissue. Here we systematically evaluated regions differently impaired by focal ischemia. Wistar rats underwent a transient 30 or 12...
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| description | Investigations following stroke first of all require information about the spatio-temporal dimension of the ischemic core as well as of perilesional and remote affected tissue. Here we systematically evaluated regions differently impaired by focal ischemia.
Wistar rats underwent a transient 30 or 120 min suture-occlusion of the middle cerebral artery (MCAO) followed by various reperfusion times (2 h, 1 d, 7 d, 30 d) or a permanent MCAO (1 d survival). Brains were characterized by TTC, thionine, and immunohistochemistry using MAP2, HSP72, and HSP27. TTC staining reliably identifies the infarct core at 1 d of reperfusion after 30 min MCAO and at all investigated times following 120 min and permanent MCAO. Nissl histology denotes the infarct core from 2 h up to 30 d after transient as well as permanent MCAO. Absent and attenuated MAP2 staining clearly identifies the infarct core and perilesional affected regions at all investigated times, respectively. HSP72 denotes perilesional areas in a limited post-ischemic time (1 d). HSP27 detects perilesional and remote impaired tissue from post-ischemic day 1 on. Furthermore a simultaneous expression of HSP72 and HSP27 in perilesional neurons was revealed.
TTC and Nissl staining can be applied to designate the infarct core. MAP2, HSP72, and HSP27 are excellent markers not only to identify perilesional and remote areas but also to discriminate affected neuronal and glial populations. Moreover markers vary in their confinement to different reperfusion times. The extent and consistency of infarcts increase with prolonged occlusion of the MCA. Therefore interindividual infarct dimension should be precisely assessed by the combined use of different markers as described in this study. |
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Wistar rats underwent a transient 30 or 120 min suture-occlusion of the middle cerebral artery (MCAO) followed by various reperfusion times (2 h, 1 d, 7 d, 30 d) or a permanent MCAO (1 d survival). Brains were characterized by TTC, thionine, and immunohistochemistry using MAP2, HSP72, and HSP27. TTC staining reliably identifies the infarct core at 1 d of reperfusion after 30 min MCAO and at all investigated times following 120 min and permanent MCAO. Nissl histology denotes the infarct core from 2 h up to 30 d after transient as well as permanent MCAO. Absent and attenuated MAP2 staining clearly identifies the infarct core and perilesional affected regions at all investigated times, respectively. HSP72 denotes perilesional areas in a limited post-ischemic time (1 d). HSP27 detects perilesional and remote impaired tissue from post-ischemic day 1 on. Furthermore a simultaneous expression of HSP72 and HSP27 in perilesional neurons was revealed.
TTC and Nissl staining can be applied to designate the infarct core. MAP2, HSP72, and HSP27 are excellent markers not only to identify perilesional and remote areas but also to discriminate affected neuronal and glial populations. Moreover markers vary in their confinement to different reperfusion times. The extent and consistency of infarcts increase with prolonged occlusion of the MCA. Therefore interindividual infarct dimension should be precisely assessed by the combined use of different markers as described in this study.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0004764</identifier><identifier>PMID: 19274095</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Biomarkers - analysis ; Blood-brain barrier ; Brain ; Brain Ischemia - pathology ; Carotid arteries ; Cerebral blood flow ; Heat shock proteins ; Histology ; HSP27 Heat-Shock Proteins - analysis ; Hsp27 protein ; HSP72 Heat-Shock Proteins - analysis ; Hsp72 protein ; Immunohistochemistry ; Infarction, Middle Cerebral Artery ; Ischemia ; Male ; Markers ; Microtubule-Associated Proteins - analysis ; Molecular weight ; Neurological Disorders/Cerebrovascular Disease ; Neurology ; Neuronal-glial interactions ; Neurons ; Neuroscience ; NMR ; Nuclear magnetic resonance ; Occlusion ; Pathology/Cellular Pathology ; Pathology/Molecular Pathology ; Pathology/Neuropathology ; Potassium ; Rats ; Rats, Wistar ; Reperfusion ; Reperfusion Injury ; Rodents ; Staining ; Staining and Labeling ; Stroke ; Stroke - pathology ; Veins & arteries</subject><ispartof>PloS one, 2009-03, Vol.4 (3), p.e4764-e4764</ispartof><rights>COPYRIGHT 2009 Public Library of Science</rights><rights>2009 Popp et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Popp et al. 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c728t-1aca08f88a5b7c4a73db075c533fc3badbd1a0c073d10c0bc67db48d54f9e5063</citedby><cites>FETCH-LOGICAL-c728t-1aca08f88a5b7c4a73db075c533fc3badbd1a0c073d10c0bc67db48d54f9e5063</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652027/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652027/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,2098,2917,23849,27907,27908,53774,53776,79351,79352</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19274095$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Kleinschnitz, Christoph</contributor><creatorcontrib>Popp, Anke</creatorcontrib><creatorcontrib>Jaenisch, Nadine</creatorcontrib><creatorcontrib>Witte, Otto W</creatorcontrib><creatorcontrib>Frahm, Christiane</creatorcontrib><title>Identification of ischemic regions in a rat model of stroke</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Investigations following stroke first of all require information about the spatio-temporal dimension of the ischemic core as well as of perilesional and remote affected tissue. Here we systematically evaluated regions differently impaired by focal ischemia.
Wistar rats underwent a transient 30 or 120 min suture-occlusion of the middle cerebral artery (MCAO) followed by various reperfusion times (2 h, 1 d, 7 d, 30 d) or a permanent MCAO (1 d survival). Brains were characterized by TTC, thionine, and immunohistochemistry using MAP2, HSP72, and HSP27. TTC staining reliably identifies the infarct core at 1 d of reperfusion after 30 min MCAO and at all investigated times following 120 min and permanent MCAO. Nissl histology denotes the infarct core from 2 h up to 30 d after transient as well as permanent MCAO. Absent and attenuated MAP2 staining clearly identifies the infarct core and perilesional affected regions at all investigated times, respectively. HSP72 denotes perilesional areas in a limited post-ischemic time (1 d). HSP27 detects perilesional and remote impaired tissue from post-ischemic day 1 on. Furthermore a simultaneous expression of HSP72 and HSP27 in perilesional neurons was revealed.
TTC and Nissl staining can be applied to designate the infarct core. MAP2, HSP72, and HSP27 are excellent markers not only to identify perilesional and remote areas but also to discriminate affected neuronal and glial populations. Moreover markers vary in their confinement to different reperfusion times. The extent and consistency of infarcts increase with prolonged occlusion of the MCA. Therefore interindividual infarct dimension should be precisely assessed by the combined use of different markers as described in this study.</description><subject>Animals</subject><subject>Biomarkers - analysis</subject><subject>Blood-brain barrier</subject><subject>Brain</subject><subject>Brain Ischemia - pathology</subject><subject>Carotid arteries</subject><subject>Cerebral blood flow</subject><subject>Heat shock proteins</subject><subject>Histology</subject><subject>HSP27 Heat-Shock Proteins - analysis</subject><subject>Hsp27 protein</subject><subject>HSP72 Heat-Shock Proteins - analysis</subject><subject>Hsp72 protein</subject><subject>Immunohistochemistry</subject><subject>Infarction, Middle Cerebral Artery</subject><subject>Ischemia</subject><subject>Male</subject><subject>Markers</subject><subject>Microtubule-Associated Proteins - analysis</subject><subject>Molecular weight</subject><subject>Neurological Disorders/Cerebrovascular Disease</subject><subject>Neurology</subject><subject>Neuronal-glial interactions</subject><subject>Neurons</subject><subject>Neuroscience</subject><subject>NMR</subject><subject>Nuclear magnetic resonance</subject><subject>Occlusion</subject><subject>Pathology/Cellular Pathology</subject><subject>Pathology/Molecular Pathology</subject><subject>Pathology/Neuropathology</subject><subject>Potassium</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion</subject><subject>Reperfusion Injury</subject><subject>Rodents</subject><subject>Staining</subject><subject>Staining and Labeling</subject><subject>Stroke</subject><subject>Stroke - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Popp, Anke</au><au>Jaenisch, Nadine</au><au>Witte, Otto W</au><au>Frahm, Christiane</au><au>Kleinschnitz, Christoph</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification of ischemic regions in a rat model of stroke</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2009-03-10</date><risdate>2009</risdate><volume>4</volume><issue>3</issue><spage>e4764</spage><epage>e4764</epage><pages>e4764-e4764</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Investigations following stroke first of all require information about the spatio-temporal dimension of the ischemic core as well as of perilesional and remote affected tissue. Here we systematically evaluated regions differently impaired by focal ischemia.
Wistar rats underwent a transient 30 or 120 min suture-occlusion of the middle cerebral artery (MCAO) followed by various reperfusion times (2 h, 1 d, 7 d, 30 d) or a permanent MCAO (1 d survival). Brains were characterized by TTC, thionine, and immunohistochemistry using MAP2, HSP72, and HSP27. TTC staining reliably identifies the infarct core at 1 d of reperfusion after 30 min MCAO and at all investigated times following 120 min and permanent MCAO. Nissl histology denotes the infarct core from 2 h up to 30 d after transient as well as permanent MCAO. Absent and attenuated MAP2 staining clearly identifies the infarct core and perilesional affected regions at all investigated times, respectively. HSP72 denotes perilesional areas in a limited post-ischemic time (1 d). HSP27 detects perilesional and remote impaired tissue from post-ischemic day 1 on. Furthermore a simultaneous expression of HSP72 and HSP27 in perilesional neurons was revealed.
TTC and Nissl staining can be applied to designate the infarct core. MAP2, HSP72, and HSP27 are excellent markers not only to identify perilesional and remote areas but also to discriminate affected neuronal and glial populations. Moreover markers vary in their confinement to different reperfusion times. The extent and consistency of infarcts increase with prolonged occlusion of the MCA. Therefore interindividual infarct dimension should be precisely assessed by the combined use of different markers as described in this study.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>19274095</pmid><doi>10.1371/journal.pone.0004764</doi><tpages>e4764</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biomarkers - analysis Blood-brain barrier Brain Brain Ischemia - pathology Carotid arteries Cerebral blood flow Heat shock proteins Histology HSP27 Heat-Shock Proteins - analysis Hsp27 protein HSP72 Heat-Shock Proteins - analysis Hsp72 protein Immunohistochemistry Infarction, Middle Cerebral Artery Ischemia Male Markers Microtubule-Associated Proteins - analysis Molecular weight Neurological Disorders/Cerebrovascular Disease Neurology Neuronal-glial interactions Neurons Neuroscience NMR Nuclear magnetic resonance Occlusion Pathology/Cellular Pathology Pathology/Molecular Pathology Pathology/Neuropathology Potassium Rats Rats, Wistar Reperfusion Reperfusion Injury Rodents Staining Staining and Labeling Stroke Stroke - pathology Veins & arteries |
| title | Identification of ischemic regions in a rat model of stroke |
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