Increased infarct size and exacerbated apoptosis in the glutathione peroxidase‐1 (Gpx‐1) knockout mouse brain in response to ischemia/reperfusion injury
Glutathione peroxidase is an antioxidant enzyme that is involved in the control of cellular oxidative state. Recently, unregulated oxidative state has been implicated as detrimental to neural cell viability and involved in both acute and chronic neurodegeneration. In this study we have addressed the...
Gespeichert in:
Veröffentlicht in: | Journal of neurochemistry 2001-09, Vol.78 (6), p.1389-1399 |
---|---|
Hauptverfasser: | , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 1399 |
---|---|
container_issue | 6 |
container_start_page | 1389 |
container_title | Journal of neurochemistry |
container_volume | 78 |
creator | Crack, Peter J. Taylor, Juliet M. Flentjar, Nicole J. De Haan, Judy Hertzog, Paul Iannello, Rocco C. Kola, Ismail |
description | Glutathione peroxidase is an antioxidant enzyme that is involved in the control of cellular oxidative state. Recently, unregulated oxidative state has been implicated as detrimental to neural cell viability and involved in both acute and chronic neurodegeneration. In this study we have addressed the importance of a functional glutathione peroxidase in a mouse ischemia/reperfusion model. Two hours of focal cerebral ischemia followed by 24 h of reperfusion was induced via the intraluminal suture method. Infarct volume was increased three‐fold in the glutathione peroxidase‐1 (Gpx‐1) –/– mouse compared with the wild‐type mouse; this was mirrored by an increase in the level of apoptosis found at 24 h in the Gpx‐1 –/– mouse compared with the wild‐type mouse. Neuronal deficit scores correlated to the histologic data. We also found that activated caspase‐3 expression is present at an earlier time point in the Gpx‐1 –/– mice when compared with the wild‐type mice, which suggests an enhanced susceptibility to apoptosis in the Gpx‐1 –/– mouse. This is the first known report of such a dramatic increase, both temporally and in level of apoptosis in a mouse stroke model. Our results suggest that Gpx‐1 plays an important regulatory role in the protection of neural cells in response to the extreme oxidative stress that is released during ischemia/reperfusion injury. |
doi_str_mv | 10.1046/j.1471-4159.2001.00535.x |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71209244</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>18208261</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5415-2083bac94e3a63f7b979a99e298511c79f1f1fb68c346b8b0558c8e39163fded3</originalsourceid><addsrcrecordid>eNqNkU2O1DAQhS0EYpqBKyBvQLBIxo6dH0tsRi0YBo1gA2vLcSq0e5I42IlIs-IIHIDTcRIqdItZgmzJJddXz896hFDOUs5kcbFPuSx5Inmu0owxnjKWizxd7pHN38Z9smEsyxLBZHZGHsW4R7CQBX9IzjjPS4Xkhvy8HmwAE6GhbmhNsBON7htQMzQUFmMh1GbCphn9OPnoImJ02gH93M2TmXbOD0BHCH5xDar8-v6D0xdX47IWL-nt4O2tnyfa-zkCrYPBadwB4ugHvJk8ddHuoHfmIgDqtHNESWT2czg8Jg9a00V4cjrPyac3rz9u3yY3H66ut5c3ic3xp0nGKlEbqyQIU4i2rFWpjFKQqSrn3Jaq5bjqorJCFnVVszyvbAVCcaQbaMQ5eX7UHYP_MkOcdI-uoOvMAGhclzxjKpPynyCv0EtWcASrI2iDjzFAq8fgehMOmjO9Rqj3ek1Kr0npNUL9J0K94OjT0xtz3UNzN3jKDIFnJ8BEa7o2mMG6eMdJLoXIK-ReHbmvroPDfxvQ795vsRC_AUnuu2w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>18208261</pqid></control><display><type>article</type><title>Increased infarct size and exacerbated apoptosis in the glutathione peroxidase‐1 (Gpx‐1) knockout mouse brain in response to ischemia/reperfusion injury</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><source>IngentaConnect Free/Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Wiley Online Library (Open Access Collection)</source><source>Free Full-Text Journals in Chemistry</source><creator>Crack, Peter J. ; Taylor, Juliet M. ; Flentjar, Nicole J. ; De Haan, Judy ; Hertzog, Paul ; Iannello, Rocco C. ; Kola, Ismail</creator><creatorcontrib>Crack, Peter J. ; Taylor, Juliet M. ; Flentjar, Nicole J. ; De Haan, Judy ; Hertzog, Paul ; Iannello, Rocco C. ; Kola, Ismail</creatorcontrib><description>Glutathione peroxidase is an antioxidant enzyme that is involved in the control of cellular oxidative state. Recently, unregulated oxidative state has been implicated as detrimental to neural cell viability and involved in both acute and chronic neurodegeneration. In this study we have addressed the importance of a functional glutathione peroxidase in a mouse ischemia/reperfusion model. Two hours of focal cerebral ischemia followed by 24 h of reperfusion was induced via the intraluminal suture method. Infarct volume was increased three‐fold in the glutathione peroxidase‐1 (Gpx‐1) –/– mouse compared with the wild‐type mouse; this was mirrored by an increase in the level of apoptosis found at 24 h in the Gpx‐1 –/– mouse compared with the wild‐type mouse. Neuronal deficit scores correlated to the histologic data. We also found that activated caspase‐3 expression is present at an earlier time point in the Gpx‐1 –/– mice when compared with the wild‐type mice, which suggests an enhanced susceptibility to apoptosis in the Gpx‐1 –/– mouse. This is the first known report of such a dramatic increase, both temporally and in level of apoptosis in a mouse stroke model. Our results suggest that Gpx‐1 plays an important regulatory role in the protection of neural cells in response to the extreme oxidative stress that is released during ischemia/reperfusion injury.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1046/j.1471-4159.2001.00535.x</identifier><identifier>PMID: 11579147</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Animals ; Apoptosis ; Biological and medical sciences ; Brain - pathology ; Brain - physiopathology ; Brain Ischemia - pathology ; Brain Ischemia - physiopathology ; Caspase 3 ; Caspases - metabolism ; Cerebral Infarction - pathology ; Cerebral Infarction - physiopathology ; cerebral ischemia ; Enzyme Activation - physiology ; Glutathione Peroxidase - genetics ; Glutathione Peroxidase - physiology ; glutathione peroxidase‐1 ; knockout mouse ; Lipid Peroxides - metabolism ; Medical sciences ; Mice ; Mice, Knockout - genetics ; Neurology ; Neurons - physiology ; oxidative stress ; Reperfusion Injury - pathology ; Reperfusion Injury - physiopathology ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Journal of neurochemistry, 2001-09, Vol.78 (6), p.1389-1399</ispartof><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5415-2083bac94e3a63f7b979a99e298511c79f1f1fb68c346b8b0558c8e39163fded3</citedby><cites>FETCH-LOGICAL-c5415-2083bac94e3a63f7b979a99e298511c79f1f1fb68c346b8b0558c8e39163fded3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1471-4159.2001.00535.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1471-4159.2001.00535.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14143358$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11579147$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Crack, Peter J.</creatorcontrib><creatorcontrib>Taylor, Juliet M.</creatorcontrib><creatorcontrib>Flentjar, Nicole J.</creatorcontrib><creatorcontrib>De Haan, Judy</creatorcontrib><creatorcontrib>Hertzog, Paul</creatorcontrib><creatorcontrib>Iannello, Rocco C.</creatorcontrib><creatorcontrib>Kola, Ismail</creatorcontrib><title>Increased infarct size and exacerbated apoptosis in the glutathione peroxidase‐1 (Gpx‐1) knockout mouse brain in response to ischemia/reperfusion injury</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>Glutathione peroxidase is an antioxidant enzyme that is involved in the control of cellular oxidative state. Recently, unregulated oxidative state has been implicated as detrimental to neural cell viability and involved in both acute and chronic neurodegeneration. In this study we have addressed the importance of a functional glutathione peroxidase in a mouse ischemia/reperfusion model. Two hours of focal cerebral ischemia followed by 24 h of reperfusion was induced via the intraluminal suture method. Infarct volume was increased three‐fold in the glutathione peroxidase‐1 (Gpx‐1) –/– mouse compared with the wild‐type mouse; this was mirrored by an increase in the level of apoptosis found at 24 h in the Gpx‐1 –/– mouse compared with the wild‐type mouse. Neuronal deficit scores correlated to the histologic data. We also found that activated caspase‐3 expression is present at an earlier time point in the Gpx‐1 –/– mice when compared with the wild‐type mice, which suggests an enhanced susceptibility to apoptosis in the Gpx‐1 –/– mouse. This is the first known report of such a dramatic increase, both temporally and in level of apoptosis in a mouse stroke model. Our results suggest that Gpx‐1 plays an important regulatory role in the protection of neural cells in response to the extreme oxidative stress that is released during ischemia/reperfusion injury.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Brain - pathology</subject><subject>Brain - physiopathology</subject><subject>Brain Ischemia - pathology</subject><subject>Brain Ischemia - physiopathology</subject><subject>Caspase 3</subject><subject>Caspases - metabolism</subject><subject>Cerebral Infarction - pathology</subject><subject>Cerebral Infarction - physiopathology</subject><subject>cerebral ischemia</subject><subject>Enzyme Activation - physiology</subject><subject>Glutathione Peroxidase - genetics</subject><subject>Glutathione Peroxidase - physiology</subject><subject>glutathione peroxidase‐1</subject><subject>knockout mouse</subject><subject>Lipid Peroxides - metabolism</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout - genetics</subject><subject>Neurology</subject><subject>Neurons - physiology</subject><subject>oxidative stress</subject><subject>Reperfusion Injury - pathology</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU2O1DAQhS0EYpqBKyBvQLBIxo6dH0tsRi0YBo1gA2vLcSq0e5I42IlIs-IIHIDTcRIqdItZgmzJJddXz896hFDOUs5kcbFPuSx5Inmu0owxnjKWizxd7pHN38Z9smEsyxLBZHZGHsW4R7CQBX9IzjjPS4Xkhvy8HmwAE6GhbmhNsBON7htQMzQUFmMh1GbCphn9OPnoImJ02gH93M2TmXbOD0BHCH5xDar8-v6D0xdX47IWL-nt4O2tnyfa-zkCrYPBadwB4ugHvJk8ddHuoHfmIgDqtHNESWT2czg8Jg9a00V4cjrPyac3rz9u3yY3H66ut5c3ic3xp0nGKlEbqyQIU4i2rFWpjFKQqSrn3Jaq5bjqorJCFnVVszyvbAVCcaQbaMQ5eX7UHYP_MkOcdI-uoOvMAGhclzxjKpPynyCv0EtWcASrI2iDjzFAq8fgehMOmjO9Rqj3ek1Kr0npNUL9J0K94OjT0xtz3UNzN3jKDIFnJ8BEa7o2mMG6eMdJLoXIK-ReHbmvroPDfxvQ795vsRC_AUnuu2w</recordid><startdate>200109</startdate><enddate>200109</enddate><creator>Crack, Peter J.</creator><creator>Taylor, Juliet M.</creator><creator>Flentjar, Nicole J.</creator><creator>De Haan, Judy</creator><creator>Hertzog, Paul</creator><creator>Iannello, Rocco C.</creator><creator>Kola, Ismail</creator><general>Blackwell Science Ltd</general><general>Blackwell</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>7X8</scope></search><sort><creationdate>200109</creationdate><title>Increased infarct size and exacerbated apoptosis in the glutathione peroxidase‐1 (Gpx‐1) knockout mouse brain in response to ischemia/reperfusion injury</title><author>Crack, Peter J. ; Taylor, Juliet M. ; Flentjar, Nicole J. ; De Haan, Judy ; Hertzog, Paul ; Iannello, Rocco C. ; Kola, Ismail</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5415-2083bac94e3a63f7b979a99e298511c79f1f1fb68c346b8b0558c8e39163fded3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Brain - pathology</topic><topic>Brain - physiopathology</topic><topic>Brain Ischemia - pathology</topic><topic>Brain Ischemia - physiopathology</topic><topic>Caspase 3</topic><topic>Caspases - metabolism</topic><topic>Cerebral Infarction - pathology</topic><topic>Cerebral Infarction - physiopathology</topic><topic>cerebral ischemia</topic><topic>Enzyme Activation - physiology</topic><topic>Glutathione Peroxidase - genetics</topic><topic>Glutathione Peroxidase - physiology</topic><topic>glutathione peroxidase‐1</topic><topic>knockout mouse</topic><topic>Lipid Peroxides - metabolism</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Knockout - genetics</topic><topic>Neurology</topic><topic>Neurons - physiology</topic><topic>oxidative stress</topic><topic>Reperfusion Injury - pathology</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Crack, Peter J.</creatorcontrib><creatorcontrib>Taylor, Juliet M.</creatorcontrib><creatorcontrib>Flentjar, Nicole J.</creatorcontrib><creatorcontrib>De Haan, Judy</creatorcontrib><creatorcontrib>Hertzog, Paul</creatorcontrib><creatorcontrib>Iannello, Rocco C.</creatorcontrib><creatorcontrib>Kola, Ismail</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>MEDLINE - Academic</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Crack, Peter J.</au><au>Taylor, Juliet M.</au><au>Flentjar, Nicole J.</au><au>De Haan, Judy</au><au>Hertzog, Paul</au><au>Iannello, Rocco C.</au><au>Kola, Ismail</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased infarct size and exacerbated apoptosis in the glutathione peroxidase‐1 (Gpx‐1) knockout mouse brain in response to ischemia/reperfusion injury</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2001-09</date><risdate>2001</risdate><volume>78</volume><issue>6</issue><spage>1389</spage><epage>1399</epage><pages>1389-1399</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>Glutathione peroxidase is an antioxidant enzyme that is involved in the control of cellular oxidative state. Recently, unregulated oxidative state has been implicated as detrimental to neural cell viability and involved in both acute and chronic neurodegeneration. In this study we have addressed the importance of a functional glutathione peroxidase in a mouse ischemia/reperfusion model. Two hours of focal cerebral ischemia followed by 24 h of reperfusion was induced via the intraluminal suture method. Infarct volume was increased three‐fold in the glutathione peroxidase‐1 (Gpx‐1) –/– mouse compared with the wild‐type mouse; this was mirrored by an increase in the level of apoptosis found at 24 h in the Gpx‐1 –/– mouse compared with the wild‐type mouse. Neuronal deficit scores correlated to the histologic data. We also found that activated caspase‐3 expression is present at an earlier time point in the Gpx‐1 –/– mice when compared with the wild‐type mice, which suggests an enhanced susceptibility to apoptosis in the Gpx‐1 –/– mouse. This is the first known report of such a dramatic increase, both temporally and in level of apoptosis in a mouse stroke model. Our results suggest that Gpx‐1 plays an important regulatory role in the protection of neural cells in response to the extreme oxidative stress that is released during ischemia/reperfusion injury.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>11579147</pmid><doi>10.1046/j.1471-4159.2001.00535.x</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0022-3042 |
ispartof | Journal of neurochemistry, 2001-09, Vol.78 (6), p.1389-1399 |
issn | 0022-3042 1471-4159 |
language | eng |
recordid | cdi_proquest_miscellaneous_71209244 |
source | MEDLINE; Access via Wiley Online Library; IngentaConnect Free/Open Access Journals; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); Free Full-Text Journals in Chemistry |
subjects | Animals Apoptosis Biological and medical sciences Brain - pathology Brain - physiopathology Brain Ischemia - pathology Brain Ischemia - physiopathology Caspase 3 Caspases - metabolism Cerebral Infarction - pathology Cerebral Infarction - physiopathology cerebral ischemia Enzyme Activation - physiology Glutathione Peroxidase - genetics Glutathione Peroxidase - physiology glutathione peroxidase‐1 knockout mouse Lipid Peroxides - metabolism Medical sciences Mice Mice, Knockout - genetics Neurology Neurons - physiology oxidative stress Reperfusion Injury - pathology Reperfusion Injury - physiopathology Vascular diseases and vascular malformations of the nervous system |
title | Increased infarct size and exacerbated apoptosis in the glutathione peroxidase‐1 (Gpx‐1) knockout mouse brain in response to ischemia/reperfusion injury |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T15%3A40%3A51IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Increased%20infarct%20size%20and%20exacerbated%20apoptosis%20in%20the%20glutathione%20peroxidase%E2%80%901%20(Gpx%E2%80%901)%20knockout%20mouse%20brain%20in%20response%20to%20ischemia/reperfusion%20injury&rft.jtitle=Journal%20of%20neurochemistry&rft.au=Crack,%20Peter%20J.&rft.date=2001-09&rft.volume=78&rft.issue=6&rft.spage=1389&rft.epage=1399&rft.pages=1389-1399&rft.issn=0022-3042&rft.eissn=1471-4159&rft.coden=JONRA9&rft_id=info:doi/10.1046/j.1471-4159.2001.00535.x&rft_dat=%3Cproquest_cross%3E18208261%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=18208261&rft_id=info:pmid/11579147&rfr_iscdi=true |