Characterization of monocyte chemoattractant protein-1 expression following a kainate model of status epilepticus
Abstract Brain injury due to seizure induces a robust inflammatory response that involves multiple factors. Although the expression of chemokines has been identified as a part of this response, there are remaining questions about their relative contribution to seizure pathogenesis. To address this,...
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| Veröffentlicht in: | Brain research 2007-11, Vol.1182, p.138-143 |
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| creator | Manley, Nathan C Bertrand, Anthony A Kinney, Kevin S Hing, Tressia C Sapolsky, Robert M |
| description | Abstract Brain injury due to seizure induces a robust inflammatory response that involves multiple factors. Although the expression of chemokines has been identified as a part of this response, there are remaining questions about their relative contribution to seizure pathogenesis. To address this, we report the expression profile of the chemokine, monocyte chemoattractant protein-1 (MCP-1, CCL2), during kainate-induced seizure in the rat hippocampus. Furthermore, we compare MCP-1 expression to the temporal profile of blood–brain barrier (BBB) permeability and immune cell recruitment at the injury site, since both of these events have been linked to MCP-1. We find that BBB permeability increased prior to upregulation of MCP-1, while MCP-1 upregulation and immune cell recruitment occurred concurrently, 7–13 h after opening of the BBB. Our findings support the following conclusions: (1) BBB opening to large proteins does not require MCP-1 upregulation; (2) Leukocyte immigration is not sufficient to induce BBB opening to large proteins; (3) MCP-1 upregulation likely mediates recruitment of macrophages/microglia and granulocytes during seizure injury, thus warranting further investigation of this chemokine. |
| doi_str_mv | 10.1016/j.brainres.2007.08.092 |
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Although the expression of chemokines has been identified as a part of this response, there are remaining questions about their relative contribution to seizure pathogenesis. To address this, we report the expression profile of the chemokine, monocyte chemoattractant protein-1 (MCP-1, CCL2), during kainate-induced seizure in the rat hippocampus. Furthermore, we compare MCP-1 expression to the temporal profile of blood–brain barrier (BBB) permeability and immune cell recruitment at the injury site, since both of these events have been linked to MCP-1. We find that BBB permeability increased prior to upregulation of MCP-1, while MCP-1 upregulation and immune cell recruitment occurred concurrently, 7–13 h after opening of the BBB. Our findings support the following conclusions: (1) BBB opening to large proteins does not require MCP-1 upregulation; (2) Leukocyte immigration is not sufficient to induce BBB opening to large proteins; (3) MCP-1 upregulation likely mediates recruitment of macrophages/microglia and granulocytes during seizure injury, thus warranting further investigation of this chemokine.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2007.08.092</identifier><identifier>PMID: 17950261</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Analysis of Variance ; Animals ; Biological and medical sciences ; Blood–brain barrier ; CD11b Antigen - metabolism ; Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges ; Chemokine CCL2 - metabolism ; Disease Models, Animal ; Epilepsy ; Evans Blue ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation - drug effects ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Hippocampus ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hippocampus - pathology ; Kainic Acid ; Leukocyte recruitment ; Male ; Medical sciences ; Monocyte chemoattractant protein-1 ; Nervous system (semeiology, syndromes) ; Neurology ; Rats ; Rats, Sprague-Dawley ; Status Epilepticus - chemically induced ; Status Epilepticus - metabolism ; Status Epilepticus - pathology ; Time Factors ; Vertebrates: nervous system and sense organs</subject><ispartof>Brain research, 2007-11, Vol.1182, p.138-143</ispartof><rights>Elsevier B.V.</rights><rights>2007 Elsevier B.V.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c548t-61e6c1f935f9de0dbf76b0c04f031ab7c92c426ae219a4806f5c7f90786f64e53</citedby><cites>FETCH-LOGICAL-c548t-61e6c1f935f9de0dbf76b0c04f031ab7c92c426ae219a4806f5c7f90786f64e53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.brainres.2007.08.092$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19867048$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17950261$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Manley, Nathan C</creatorcontrib><creatorcontrib>Bertrand, Anthony A</creatorcontrib><creatorcontrib>Kinney, Kevin S</creatorcontrib><creatorcontrib>Hing, Tressia C</creatorcontrib><creatorcontrib>Sapolsky, Robert M</creatorcontrib><title>Characterization of monocyte chemoattractant protein-1 expression following a kainate model of status epilepticus</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Abstract Brain injury due to seizure induces a robust inflammatory response that involves multiple factors. Although the expression of chemokines has been identified as a part of this response, there are remaining questions about their relative contribution to seizure pathogenesis. To address this, we report the expression profile of the chemokine, monocyte chemoattractant protein-1 (MCP-1, CCL2), during kainate-induced seizure in the rat hippocampus. Furthermore, we compare MCP-1 expression to the temporal profile of blood–brain barrier (BBB) permeability and immune cell recruitment at the injury site, since both of these events have been linked to MCP-1. We find that BBB permeability increased prior to upregulation of MCP-1, while MCP-1 upregulation and immune cell recruitment occurred concurrently, 7–13 h after opening of the BBB. Our findings support the following conclusions: (1) BBB opening to large proteins does not require MCP-1 upregulation; (2) Leukocyte immigration is not sufficient to induce BBB opening to large proteins; (3) MCP-1 upregulation likely mediates recruitment of macrophages/microglia and granulocytes during seizure injury, thus warranting further investigation of this chemokine.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood–brain barrier</subject><subject>CD11b Antigen - metabolism</subject><subject>Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Disease Models, Animal</subject><subject>Epilepsy</subject><subject>Evans Blue</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Hippocampus</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>Kainic Acid</subject><subject>Leukocyte recruitment</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Monocyte chemoattractant protein-1</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Status Epilepticus - chemically induced</subject><subject>Status Epilepticus - metabolism</subject><subject>Status Epilepticus - pathology</subject><subject>Time Factors</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk2L1TAUhosoznX0Lwzd6K71JG3TZCPKxS8YcKGuQ5qeOLnTJp0kHb3-elPulQE3rkLged9zeDhFcUWgJkDY60M9BGVdwFhTgL4GXoOgj4od4T2tGG3hcbEDAFZxIZqL4lmMh_xtGgFPiwvSiw4oI7vibn-jgtIJg_2tkvWu9KacvfP6mLDUNzh7ldJGKJfKJfiE1lWkxF9Lnh23gPHT5H9a96NU5W3eSeXg7EectqqYVFpjiYudcElWr_F58cSoKeKL83tZfP_w_tv-U3X95ePn_bvrSnctTxUjyDQxoumMGBHGwfRsAA2tgYaoodeC6pYyhZQI1XJgptO9EdBzZliLXXNZvDr15qXvVoxJzjZqnCbl0K9RUmhbQboNZCdQBx9jQCOXYGcVjpKA3GTLg_wrW26yJXCZZefg1XnCOsw4PsTOdjPw8gyoqNVkgnLaxgdOcNZDyzP39sRh9nFvMcioLTqNow2okxy9_f8ub_6p0JN1Nk-9xSPGg1-Dy7YlkZFKkF-309guA3qgpOW8-QNnPriN</recordid><startdate>20071128</startdate><enddate>20071128</enddate><creator>Manley, Nathan C</creator><creator>Bertrand, Anthony A</creator><creator>Kinney, Kevin S</creator><creator>Hing, Tressia C</creator><creator>Sapolsky, Robert M</creator><general>Elsevier B.V</general><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>7TK</scope></search><sort><creationdate>20071128</creationdate><title>Characterization of monocyte chemoattractant protein-1 expression following a kainate model of status epilepticus</title><author>Manley, Nathan C ; Bertrand, Anthony A ; Kinney, Kevin S ; Hing, Tressia C ; Sapolsky, Robert M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c548t-61e6c1f935f9de0dbf76b0c04f031ab7c92c426ae219a4806f5c7f90786f64e53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood–brain barrier</topic><topic>CD11b Antigen - metabolism</topic><topic>Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Disease Models, Animal</topic><topic>Epilepsy</topic><topic>Evans Blue</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Hippocampus</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - pathology</topic><topic>Kainic Acid</topic><topic>Leukocyte recruitment</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Monocyte chemoattractant protein-1</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Status Epilepticus - chemically induced</topic><topic>Status Epilepticus - metabolism</topic><topic>Status Epilepticus - pathology</topic><topic>Time Factors</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Manley, Nathan C</creatorcontrib><creatorcontrib>Bertrand, Anthony A</creatorcontrib><creatorcontrib>Kinney, Kevin S</creatorcontrib><creatorcontrib>Hing, Tressia C</creatorcontrib><creatorcontrib>Sapolsky, Robert M</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><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Manley, Nathan C</au><au>Bertrand, Anthony A</au><au>Kinney, Kevin S</au><au>Hing, Tressia C</au><au>Sapolsky, Robert M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Characterization of monocyte chemoattractant protein-1 expression following a kainate model of status epilepticus</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2007-11-28</date><risdate>2007</risdate><volume>1182</volume><spage>138</spage><epage>143</epage><pages>138-143</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Abstract Brain injury due to seizure induces a robust inflammatory response that involves multiple factors. Although the expression of chemokines has been identified as a part of this response, there are remaining questions about their relative contribution to seizure pathogenesis. To address this, we report the expression profile of the chemokine, monocyte chemoattractant protein-1 (MCP-1, CCL2), during kainate-induced seizure in the rat hippocampus. Furthermore, we compare MCP-1 expression to the temporal profile of blood–brain barrier (BBB) permeability and immune cell recruitment at the injury site, since both of these events have been linked to MCP-1. We find that BBB permeability increased prior to upregulation of MCP-1, while MCP-1 upregulation and immune cell recruitment occurred concurrently, 7–13 h after opening of the BBB. Our findings support the following conclusions: (1) BBB opening to large proteins does not require MCP-1 upregulation; (2) Leukocyte immigration is not sufficient to induce BBB opening to large proteins; (3) MCP-1 upregulation likely mediates recruitment of macrophages/microglia and granulocytes during seizure injury, thus warranting further investigation of this chemokine.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>17950261</pmid><doi>10.1016/j.brainres.2007.08.092</doi><tpages>6</tpages></addata></record> |
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| subjects | Analysis of Variance Animals Biological and medical sciences Blood–brain barrier CD11b Antigen - metabolism Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges Chemokine CCL2 - metabolism Disease Models, Animal Epilepsy Evans Blue Fundamental and applied biological sciences. Psychology Gene Expression Regulation - drug effects Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Hippocampus Hippocampus - drug effects Hippocampus - metabolism Hippocampus - pathology Kainic Acid Leukocyte recruitment Male Medical sciences Monocyte chemoattractant protein-1 Nervous system (semeiology, syndromes) Neurology Rats Rats, Sprague-Dawley Status Epilepticus - chemically induced Status Epilepticus - metabolism Status Epilepticus - pathology Time Factors Vertebrates: nervous system and sense organs |
| title | Characterization of monocyte chemoattractant protein-1 expression following a kainate model of status epilepticus |
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