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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| Published in | The Journal of biological chemistry Vol. 278; no. 44; pp. 43807 - 43817 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
31.10.2003
American Society for Biochemistry and Molecular Biology |
| Subjects | |
| Online Access | Get full text |
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| 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. |
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| AbstractList | 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 17 R -resolvins. The newly discovered brain messenger 10,17 S -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. 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, NF Kappa B, 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- beta -induced NF Kappa B 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. 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. 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, NFkappaB, 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-beta-induced NFkappaB 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. |
| Author | Lukiw, Walter J. Gronert, Karsten Chiang, Nan Tian, Xiao Hua Hardy, Mattie Gimenez, Juan M. Marcheselli, Victor L. Bazan, Nicolas G. Musto, Alberto Serhan, Charles N. Hong, Song |
| Author_xml | – sequence: 1 givenname: Victor L. surname: Marcheselli fullname: Marcheselli, Victor L. organization: Neuroscience Center of Excellence and Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112 – sequence: 2 givenname: Song surname: Hong fullname: Hong, Song organization: Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115 – sequence: 3 givenname: Walter J. surname: Lukiw fullname: Lukiw, Walter J. organization: Neuroscience Center of Excellence and Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112 – sequence: 4 givenname: Xiao Hua surname: Tian fullname: Tian, Xiao Hua organization: Neuroscience Center of Excellence and Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112 – sequence: 5 givenname: Karsten surname: Gronert fullname: Gronert, Karsten organization: Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115 – sequence: 6 givenname: Alberto surname: Musto fullname: Musto, Alberto organization: Neuroscience Center of Excellence and Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112 – sequence: 7 givenname: Mattie surname: Hardy fullname: Hardy, Mattie organization: Neuroscience Center of Excellence and Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112 – sequence: 8 givenname: Juan M. surname: Gimenez fullname: Gimenez, Juan M. organization: Neuroscience Center of Excellence and Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112 – sequence: 9 givenname: Nan surname: Chiang fullname: Chiang, Nan organization: Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115 – sequence: 10 givenname: Charles N. surname: Serhan fullname: Serhan, Charles N. organization: Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115 – sequence: 11 givenname: Nicolas G. surname: Bazan fullname: Bazan, Nicolas G. email: nbazan@lsuhsc.edu organization: Neuroscience Center of Excellence and Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112 |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/12923200$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:19654788$$DView record from Swedish Publication Index |
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| Snippet | Ischemic stroke triggers lipid peroxidation and neuronal injury. Docosahexaenoic acid released from membrane phospholipids during brain ischemia is a major... Ischemic stroke triggers lipid peroxidation and neuronal injury. Docosahexaenoic acid released from membrane phospholipids during brain ischemia is a major... |
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| SubjectTerms | 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 Medicin och hälsovetenskap 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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