Novel Docosanoids Inhibit Brain Ischemia-Reperfusion-mediated Leukocyte Infiltration and Pro-inflammatory Gene Expression
Ischemic stroke triggers lipid peroxidation and neuronal injury. Docosahexaenoic acid released from membrane phospholipids during brain ischemia is a major source of lipid peroxides. Leukocyte infiltration and pro-inflammatory gene expression also contribute to stroke damage. In this study using lip...
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| Veröffentlicht in: | The Journal of biological chemistry 2003-10, Vol.278 (44), p.43807-43817 |
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| creator | Marcheselli, Victor L. Hong, Song Lukiw, Walter J. Tian, Xiao Hua Gronert, Karsten Musto, Alberto Hardy, Mattie Gimenez, Juan M. Chiang, Nan Serhan, Charles N. Bazan, Nicolas G. |
| description | Ischemic stroke triggers lipid peroxidation and neuronal injury. Docosahexaenoic acid released from membrane phospholipids during brain ischemia is a major source of lipid peroxides. Leukocyte infiltration and pro-inflammatory gene expression also contribute to stroke damage. In this study using lipidomic analysis, we have identified stereospecific messengers from docosahexaenoate-oxygenation pathways in a mouse stroke model. Aspirin, widely used to prevent cerebrovascular disease, activates an additional pathway, which includes the 17R-resolvins. The newly discovered brain messenger 10,17S-docosatriene potently inhibited leukocyte infiltration, NFκB, and cyclooxygenase-2 induction in experimental stroke and elicited neuroprotection. In addition, in neural cells in culture, this lipid messenger also inhibited both interleukin 1-β-induced NFκB activation and cyclooxygenase-2 expression. Thus, the specific novel bioactive docosanoids generated in vivo counteract leukocyte-mediated injury as well as pro-inflammatory gene induction. These results challenge the view that docosahexaenoate only participates in brain damage and demonstrate that this fatty acid is also the endogenous precursor to a neuroprotective signaling response to ischemia-reperfusion. |
| doi_str_mv | 10.1074/jbc.M305841200 |
| format | Article |
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Docosahexaenoic acid released from membrane phospholipids during brain ischemia is a major source of lipid peroxides. Leukocyte infiltration and pro-inflammatory gene expression also contribute to stroke damage. In this study using lipidomic analysis, we have identified stereospecific messengers from docosahexaenoate-oxygenation pathways in a mouse stroke model. Aspirin, widely used to prevent cerebrovascular disease, activates an additional pathway, which includes the 17R-resolvins. The newly discovered brain messenger 10,17S-docosatriene potently inhibited leukocyte infiltration, NFκB, and cyclooxygenase-2 induction in experimental stroke and elicited neuroprotection. In addition, in neural cells in culture, this lipid messenger also inhibited both interleukin 1-β-induced NFκB activation and cyclooxygenase-2 expression. Thus, the specific novel bioactive docosanoids generated in vivo counteract leukocyte-mediated injury as well as pro-inflammatory gene induction. These results challenge the view that docosahexaenoate only participates in brain damage and demonstrate that this fatty acid is also the endogenous precursor to a neuroprotective signaling response to ischemia-reperfusion.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M305841200</identifier><identifier>PMID: 12923200</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Anti-Inflammatory Agents, Non-Steroidal - pharmacology ; Aspirin - pharmacology ; Brain - pathology ; Cells, Cultured ; Cerebral Arteries - pathology ; Cyclooxygenase 2 ; Docosahexaenoic Acids - chemistry ; Docosahexaenoic Acids - pharmacology ; docosanoids ; Hippocampus - metabolism ; Humans ; Immunohistochemistry ; Interleukin-1 - metabolism ; Isoenzymes - metabolism ; Leukocytes - metabolism ; Leukocytes - pathology ; Lipid Peroxidation ; Membrane Proteins ; Mice ; Microscopy, Fluorescence ; Models, Chemical ; Neurons - metabolism ; NF-kappa B - metabolism ; Prostaglandin-Endoperoxide Synthases - metabolism ; Reperfusion Injury ; Signal Transduction ; Stem Cells - metabolism ; Time Factors</subject><ispartof>The Journal of biological chemistry, 2003-10, Vol.278 (44), p.43807-43817</ispartof><rights>2003 © 2003 ASBMB. 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Docosahexaenoic acid released from membrane phospholipids during brain ischemia is a major source of lipid peroxides. Leukocyte infiltration and pro-inflammatory gene expression also contribute to stroke damage. In this study using lipidomic analysis, we have identified stereospecific messengers from docosahexaenoate-oxygenation pathways in a mouse stroke model. Aspirin, widely used to prevent cerebrovascular disease, activates an additional pathway, which includes the 17R-resolvins. The newly discovered brain messenger 10,17S-docosatriene potently inhibited leukocyte infiltration, NFκB, and cyclooxygenase-2 induction in experimental stroke and elicited neuroprotection. In addition, in neural cells in culture, this lipid messenger also inhibited both interleukin 1-β-induced NFκB activation and cyclooxygenase-2 expression. Thus, the specific novel bioactive docosanoids generated in vivo counteract leukocyte-mediated injury as well as pro-inflammatory gene induction. These results challenge the view that docosahexaenoate only participates in brain damage and demonstrate that this fatty acid is also the endogenous precursor to a neuroprotective signaling response to ischemia-reperfusion.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</subject><subject>Aspirin - pharmacology</subject><subject>Brain - pathology</subject><subject>Cells, Cultured</subject><subject>Cerebral Arteries - pathology</subject><subject>Cyclooxygenase 2</subject><subject>Docosahexaenoic Acids - chemistry</subject><subject>Docosahexaenoic Acids - pharmacology</subject><subject>docosanoids</subject><subject>Hippocampus - metabolism</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Interleukin-1 - metabolism</subject><subject>Isoenzymes - metabolism</subject><subject>Leukocytes - metabolism</subject><subject>Leukocytes - pathology</subject><subject>Lipid Peroxidation</subject><subject>Membrane Proteins</subject><subject>Mice</subject><subject>Microscopy, Fluorescence</subject><subject>Models, Chemical</subject><subject>Neurons - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Prostaglandin-Endoperoxide Synthases - metabolism</subject><subject>Reperfusion Injury</subject><subject>Signal Transduction</subject><subject>Stem Cells - metabolism</subject><subject>Time Factors</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtvEzEURi0EomnLliXyArGbcG3Pw15CKSVSeKhqJXaWx3NNXGbGqT1Tmn-Po0TqCuGNFz730_V3CHnNYMmgKd_ftXb5VUAlS8YBnpEFAykKUbGfz8kCgLNC8UqekNOU7iCfUrGX5IRxxUXmF2T3LTxgTz8FG5IZg-8SXY0b3_qJfozGj3SV7AYHb4pr3GJ0c_JhLAbsvJmwo2ucfwe7mzBPOd9P0Uz5nZqxoz9iKPzoejMMZgpxR69wRHr5uI2Y9iHn5IUzfcJXx_uM3H6-vLn4Uqy_X60uPqwLWwJMhemwghLqClomuwoZtKq1pbVcVUq6ToFrpHUcatNi_l0tHBcNVrVTHSjZiDPy7pC7jeF-xjTpwSeLfW9GDHPSDROiqdT_QSZVDXXNMrg8gDaGlCI6vY1-MHGnGei9FZ2t6CcreeDNMXluc3VP-FFDBt4egI3_tfnjI-rWh33vmjdSl6UuhYT9hvKAYe7rwWPUyXocbbYR0U66C_5fK_wFj6CohQ</recordid><startdate>20031031</startdate><enddate>20031031</enddate><creator>Marcheselli, Victor L.</creator><creator>Hong, Song</creator><creator>Lukiw, Walter J.</creator><creator>Tian, Xiao Hua</creator><creator>Gronert, Karsten</creator><creator>Musto, Alberto</creator><creator>Hardy, Mattie</creator><creator>Gimenez, Juan M.</creator><creator>Chiang, Nan</creator><creator>Serhan, Charles N.</creator><creator>Bazan, Nicolas G.</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20031031</creationdate><title>Novel Docosanoids Inhibit Brain Ischemia-Reperfusion-mediated Leukocyte Infiltration and Pro-inflammatory Gene Expression</title><author>Marcheselli, Victor L. ; Hong, Song ; Lukiw, Walter J. ; Tian, Xiao Hua ; Gronert, Karsten ; Musto, Alberto ; Hardy, Mattie ; Gimenez, Juan M. ; Chiang, Nan ; Serhan, Charles N. ; Bazan, Nicolas G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c400t-ade5040650b18d5e10b9bc4cc29598fd90f78cf206abe49163f237e56f9d09873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</topic><topic>Aspirin - pharmacology</topic><topic>Brain - pathology</topic><topic>Cells, Cultured</topic><topic>Cerebral Arteries - pathology</topic><topic>Cyclooxygenase 2</topic><topic>Docosahexaenoic Acids - chemistry</topic><topic>Docosahexaenoic Acids - pharmacology</topic><topic>docosanoids</topic><topic>Hippocampus - metabolism</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Interleukin-1 - metabolism</topic><topic>Isoenzymes - metabolism</topic><topic>Leukocytes - metabolism</topic><topic>Leukocytes - pathology</topic><topic>Lipid Peroxidation</topic><topic>Membrane Proteins</topic><topic>Mice</topic><topic>Microscopy, Fluorescence</topic><topic>Models, Chemical</topic><topic>Neurons - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Prostaglandin-Endoperoxide Synthases - metabolism</topic><topic>Reperfusion Injury</topic><topic>Signal Transduction</topic><topic>Stem Cells - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marcheselli, Victor L.</creatorcontrib><creatorcontrib>Hong, Song</creatorcontrib><creatorcontrib>Lukiw, Walter J.</creatorcontrib><creatorcontrib>Tian, Xiao Hua</creatorcontrib><creatorcontrib>Gronert, Karsten</creatorcontrib><creatorcontrib>Musto, Alberto</creatorcontrib><creatorcontrib>Hardy, Mattie</creatorcontrib><creatorcontrib>Gimenez, Juan M.</creatorcontrib><creatorcontrib>Chiang, Nan</creatorcontrib><creatorcontrib>Serhan, Charles N.</creatorcontrib><creatorcontrib>Bazan, Nicolas G.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marcheselli, Victor L.</au><au>Hong, Song</au><au>Lukiw, Walter J.</au><au>Tian, Xiao Hua</au><au>Gronert, Karsten</au><au>Musto, Alberto</au><au>Hardy, Mattie</au><au>Gimenez, Juan M.</au><au>Chiang, Nan</au><au>Serhan, Charles N.</au><au>Bazan, Nicolas G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Novel Docosanoids Inhibit Brain Ischemia-Reperfusion-mediated Leukocyte Infiltration and Pro-inflammatory Gene Expression</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2003-10-31</date><risdate>2003</risdate><volume>278</volume><issue>44</issue><spage>43807</spage><epage>43817</epage><pages>43807-43817</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Ischemic stroke triggers lipid peroxidation and neuronal injury. Docosahexaenoic acid released from membrane phospholipids during brain ischemia is a major source of lipid peroxides. Leukocyte infiltration and pro-inflammatory gene expression also contribute to stroke damage. In this study using lipidomic analysis, we have identified stereospecific messengers from docosahexaenoate-oxygenation pathways in a mouse stroke model. Aspirin, widely used to prevent cerebrovascular disease, activates an additional pathway, which includes the 17R-resolvins. The newly discovered brain messenger 10,17S-docosatriene potently inhibited leukocyte infiltration, NFκB, and cyclooxygenase-2 induction in experimental stroke and elicited neuroprotection. In addition, in neural cells in culture, this lipid messenger also inhibited both interleukin 1-β-induced NFκB activation and cyclooxygenase-2 expression. Thus, the specific novel bioactive docosanoids generated in vivo counteract leukocyte-mediated injury as well as pro-inflammatory gene induction. These results challenge the view that docosahexaenoate only participates in brain damage and demonstrate that this fatty acid is also the endogenous precursor to a neuroprotective signaling response to ischemia-reperfusion.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12923200</pmid><doi>10.1074/jbc.M305841200</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anti-Inflammatory Agents, Non-Steroidal - pharmacology Aspirin - pharmacology Brain - pathology Cells, Cultured Cerebral Arteries - pathology Cyclooxygenase 2 Docosahexaenoic Acids - chemistry Docosahexaenoic Acids - pharmacology docosanoids Hippocampus - metabolism Humans Immunohistochemistry Interleukin-1 - metabolism Isoenzymes - metabolism Leukocytes - metabolism Leukocytes - pathology Lipid Peroxidation Membrane Proteins Mice Microscopy, Fluorescence Models, Chemical Neurons - metabolism NF-kappa B - metabolism Prostaglandin-Endoperoxide Synthases - metabolism Reperfusion Injury Signal Transduction Stem Cells - metabolism Time Factors |
| title | Novel Docosanoids Inhibit Brain Ischemia-Reperfusion-mediated Leukocyte Infiltration and Pro-inflammatory Gene Expression |
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