Neuronal expression of peroxisome proliferator-activated receptor-gamma (PPARγ) and 15d-prostaglandin J2 : Mediated protection of brain after experimental cerebral ischemia in rat
Existing experimental evidence suggests that PPARgamma may play a beneficial role in neuroprotection from various brain pathologies. Here we found that focal cerebral ischemia induced by middle cerebral/common carotid arteries occlusion (MCA/CCAo) induced up-regulation of PPARgamma messenger RNA in...
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| Veröffentlicht in: | Brain research 2006-06, Vol.1096 (1), p.196-203 |
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| creator | ZHISHUO OU XIURONG ZHAO LABICHE, Lise A STRONG, Roger GROTTA, James C HERRMANN, Oliver ARONOWSKI, Jaroslaw |
| description | Existing experimental evidence suggests that PPARgamma may play a beneficial role in neuroprotection from various brain pathologies. Here we found that focal cerebral ischemia induced by middle cerebral/common carotid arteries occlusion (MCA/CCAo) induced up-regulation of PPARgamma messenger RNA in the ischemic hemisphere as early as 6 h after the ischemic event. The increased PPARgamma mRNA expression was primarily associated with neurons in the ischemic penumbra, suggesting an important role for PPARgamma in neurons after ischemia. Intraventricular injection of 15d-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a proposed endogenous PPARgamma agonist, into the ischemic rat brains significantly increased the PPARgamma-DNA-binding activity and reduced infarction volume at 24 h after reperfusion. We propose that PPARgamma up-regulation in response to ischemia may contribute to PPARgamma activation in the presence of PPARgamma agonists. Activation of PPARgamma in neurons at an early stage after ischemia may represent a pro-survival mechanism against ischemic injury. |
| doi_str_mv | 10.1016/j.brainres.2006.04.062 |
| format | Article |
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Here we found that focal cerebral ischemia induced by middle cerebral/common carotid arteries occlusion (MCA/CCAo) induced up-regulation of PPARgamma messenger RNA in the ischemic hemisphere as early as 6 h after the ischemic event. The increased PPARgamma mRNA expression was primarily associated with neurons in the ischemic penumbra, suggesting an important role for PPARgamma in neurons after ischemia. Intraventricular injection of 15d-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a proposed endogenous PPARgamma agonist, into the ischemic rat brains significantly increased the PPARgamma-DNA-binding activity and reduced infarction volume at 24 h after reperfusion. We propose that PPARgamma up-regulation in response to ischemia may contribute to PPARgamma activation in the presence of PPARgamma agonists. Activation of PPARgamma in neurons at an early stage after ischemia may represent a pro-survival mechanism against ischemic injury.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2006.04.062</identifier><identifier>PMID: 16725118</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier</publisher><subject>Animals ; Biological and medical sciences ; Brain - pathology ; Brain Ischemia - drug therapy ; Brain Ischemia - pathology ; Cerebral Infarction - drug therapy ; Cerebral Infarction - pathology ; Electrophoretic Mobility Shift Assay ; In Situ Hybridization ; Injections, Intraventricular ; Male ; Medical sciences ; Neurology ; Neurons - metabolism ; Neuroprotective Agents ; PPAR gamma - agonists ; PPAR gamma - biosynthesis ; Prostaglandin D2 - administration & dosage ; Prostaglandin D2 - analogs & derivatives ; Prostaglandin D2 - pharmacology ; Rats ; Rats, Long-Evans ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - biosynthesis ; Up-Regulation - physiology ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Brain research, 2006-06, Vol.1096 (1), p.196-203</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c320t-ae3728d69218bbd07a889cdaf3fd6b0ca7178f319dc70b916f20b713e7e5c31b3</citedby><cites>FETCH-LOGICAL-c320t-ae3728d69218bbd07a889cdaf3fd6b0ca7178f319dc70b916f20b713e7e5c31b3</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=17919521$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16725118$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ZHISHUO OU</creatorcontrib><creatorcontrib>XIURONG ZHAO</creatorcontrib><creatorcontrib>LABICHE, Lise A</creatorcontrib><creatorcontrib>STRONG, Roger</creatorcontrib><creatorcontrib>GROTTA, James C</creatorcontrib><creatorcontrib>HERRMANN, Oliver</creatorcontrib><creatorcontrib>ARONOWSKI, Jaroslaw</creatorcontrib><title>Neuronal expression of peroxisome proliferator-activated receptor-gamma (PPARγ) and 15d-prostaglandin J2 : Mediated protection of brain after experimental cerebral ischemia in rat</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Existing experimental evidence suggests that PPARgamma may play a beneficial role in neuroprotection from various brain pathologies. Here we found that focal cerebral ischemia induced by middle cerebral/common carotid arteries occlusion (MCA/CCAo) induced up-regulation of PPARgamma messenger RNA in the ischemic hemisphere as early as 6 h after the ischemic event. The increased PPARgamma mRNA expression was primarily associated with neurons in the ischemic penumbra, suggesting an important role for PPARgamma in neurons after ischemia. Intraventricular injection of 15d-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a proposed endogenous PPARgamma agonist, into the ischemic rat brains significantly increased the PPARgamma-DNA-binding activity and reduced infarction volume at 24 h after reperfusion. We propose that PPARgamma up-regulation in response to ischemia may contribute to PPARgamma activation in the presence of PPARgamma agonists. Activation of PPARgamma in neurons at an early stage after ischemia may represent a pro-survival mechanism against ischemic injury.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain - pathology</subject><subject>Brain Ischemia - drug therapy</subject><subject>Brain Ischemia - pathology</subject><subject>Cerebral Infarction - drug therapy</subject><subject>Cerebral Infarction - pathology</subject><subject>Electrophoretic Mobility Shift Assay</subject><subject>In Situ Hybridization</subject><subject>Injections, Intraventricular</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Neurons - metabolism</subject><subject>Neuroprotective Agents</subject><subject>PPAR gamma - agonists</subject><subject>PPAR gamma - biosynthesis</subject><subject>Prostaglandin D2 - administration & dosage</subject><subject>Prostaglandin D2 - analogs & derivatives</subject><subject>Prostaglandin D2 - pharmacology</subject><subject>Rats</subject><subject>Rats, Long-Evans</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Up-Regulation - physiology</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFUctuFDEQtBCILIFfiHwBwWEGP3bsGW5RxFMBIgRnq8duB6_msdizKHwXfAffRG92UU5Wu6q6q1SMnUlRSyHNy03dZ0hTxlIrIUwt1rUw6h5bydaqyqi1uM9WgpCq7Tp9wh6VsqFR6048ZCfSWNVI2a7Yn0-4y_MEA8ebLW0raZ74HPkW83yTyjwi3-Z5SBEzLHOuwC_pJywYeEaP2_3XNYwj8OdXV-df_v5-wWEKXDahIllZ4HqgOU38g-Kv-EcM6VZL2IK06XDrNgmHuGDeu8CcRpwWsuQxI4EDT8V_xzEBJx75eMweRBgKPjm-p-zbm9dfL95Vl5_fvr84v6y8VmKpALVVbTCdkm3fB2GhbTsfIOoYTC88WGnbqGUXvBV9J01UordSo8XGa9nrU_bssJf8_thhWdxITnCgTDjvijOtEbKxDRHNgegpdMkY3ZZCQP7lpHD7vtzG_e_L7ftyYu2oLxKeHS_s-hHDnexYEBGeHglQPAwxw-RTuePZTnaNkvoffL2l6Q</recordid><startdate>20060622</startdate><enddate>20060622</enddate><creator>ZHISHUO OU</creator><creator>XIURONG ZHAO</creator><creator>LABICHE, Lise A</creator><creator>STRONG, Roger</creator><creator>GROTTA, James C</creator><creator>HERRMANN, Oliver</creator><creator>ARONOWSKI, Jaroslaw</creator><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>7X8</scope></search><sort><creationdate>20060622</creationdate><title>Neuronal expression of peroxisome proliferator-activated receptor-gamma (PPARγ) and 15d-prostaglandin J2 : Mediated protection of brain after experimental cerebral ischemia in rat</title><author>ZHISHUO OU ; XIURONG ZHAO ; LABICHE, Lise A ; STRONG, Roger ; GROTTA, James C ; HERRMANN, Oliver ; ARONOWSKI, Jaroslaw</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c320t-ae3728d69218bbd07a889cdaf3fd6b0ca7178f319dc70b916f20b713e7e5c31b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain - pathology</topic><topic>Brain Ischemia - drug therapy</topic><topic>Brain Ischemia - pathology</topic><topic>Cerebral Infarction - drug therapy</topic><topic>Cerebral Infarction - pathology</topic><topic>Electrophoretic Mobility Shift Assay</topic><topic>In Situ Hybridization</topic><topic>Injections, Intraventricular</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>Neurons - metabolism</topic><topic>Neuroprotective Agents</topic><topic>PPAR gamma - agonists</topic><topic>PPAR gamma - biosynthesis</topic><topic>Prostaglandin D2 - administration & dosage</topic><topic>Prostaglandin D2 - analogs & derivatives</topic><topic>Prostaglandin D2 - pharmacology</topic><topic>Rats</topic><topic>Rats, Long-Evans</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - biosynthesis</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>ZHISHUO OU</creatorcontrib><creatorcontrib>XIURONG ZHAO</creatorcontrib><creatorcontrib>LABICHE, Lise A</creatorcontrib><creatorcontrib>STRONG, Roger</creatorcontrib><creatorcontrib>GROTTA, James C</creatorcontrib><creatorcontrib>HERRMANN, Oliver</creatorcontrib><creatorcontrib>ARONOWSKI, Jaroslaw</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>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ZHISHUO OU</au><au>XIURONG ZHAO</au><au>LABICHE, Lise A</au><au>STRONG, Roger</au><au>GROTTA, James C</au><au>HERRMANN, Oliver</au><au>ARONOWSKI, Jaroslaw</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuronal expression of peroxisome proliferator-activated receptor-gamma (PPARγ) and 15d-prostaglandin J2 : Mediated protection of brain after experimental cerebral ischemia in rat</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2006-06-22</date><risdate>2006</risdate><volume>1096</volume><issue>1</issue><spage>196</spage><epage>203</epage><pages>196-203</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Existing experimental evidence suggests that PPARgamma may play a beneficial role in neuroprotection from various brain pathologies. Here we found that focal cerebral ischemia induced by middle cerebral/common carotid arteries occlusion (MCA/CCAo) induced up-regulation of PPARgamma messenger RNA in the ischemic hemisphere as early as 6 h after the ischemic event. The increased PPARgamma mRNA expression was primarily associated with neurons in the ischemic penumbra, suggesting an important role for PPARgamma in neurons after ischemia. Intraventricular injection of 15d-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a proposed endogenous PPARgamma agonist, into the ischemic rat brains significantly increased the PPARgamma-DNA-binding activity and reduced infarction volume at 24 h after reperfusion. We propose that PPARgamma up-regulation in response to ischemia may contribute to PPARgamma activation in the presence of PPARgamma agonists. Activation of PPARgamma in neurons at an early stage after ischemia may represent a pro-survival mechanism against ischemic injury.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier</pub><pmid>16725118</pmid><doi>10.1016/j.brainres.2006.04.062</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Brain - pathology Brain Ischemia - drug therapy Brain Ischemia - pathology Cerebral Infarction - drug therapy Cerebral Infarction - pathology Electrophoretic Mobility Shift Assay In Situ Hybridization Injections, Intraventricular Male Medical sciences Neurology Neurons - metabolism Neuroprotective Agents PPAR gamma - agonists PPAR gamma - biosynthesis Prostaglandin D2 - administration & dosage Prostaglandin D2 - analogs & derivatives Prostaglandin D2 - pharmacology Rats Rats, Long-Evans Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - biosynthesis Up-Regulation - physiology Vascular diseases and vascular malformations of the nervous system |
| title | Neuronal expression of peroxisome proliferator-activated receptor-gamma (PPARγ) and 15d-prostaglandin J2 : Mediated protection of brain after experimental cerebral ischemia in rat |
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