Abstract |
After complement system (CS) activation, the sequential production of complement products increases cell injury and death through opsonophagocytosis, cytolysis, adaptive, and inflammatory cell responses. These responses potentiate cerebral ischemia-reperfusion (IR) injury after ischemic stroke and reperfusion. Activation of the CS via mannose binding lectin (MBL)-initiated lectin pathway is known to increase tissue damage in response to IR in muscle, myocardium and intestine tissue. In contrast, the contribution of this pathway to cerebral IR injury, a neutrophil-mediated event, is less clear. Therefore, we investigated the potential protective role of MBL deficiency in neutrophil-mediated cerebral injury after IR. Using an intraluminal filament method, neutrophil activation and cerebral injury were compared between MBL-deficient and wild type C57Bl/6 mice subjected to 60 minutes of MCA ischemia and reperfusion. Systemic neutrophil activation was not decreased in MBL-deficient animals after IR. In MBL-deficient animals, cerebral injury was significantly decreased only in the striatum (p < 0.05). Despite MBL deficiency, C3 depositions were evident in the injured hemisphere during reperfusion. These results indicate that while MBL deficiency results in a modest protection of a sub-cortical brain region during IR, redundant complement pathway activation may overwhelm further beneficial effects of MBL deficiency during reperfusion.
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Authors | Helena Morrison, Jennifer Frye, Grace Davis-Gorman, Janet Funk, Paul McDonagh, Gregory Stahl, Leslie Ritter |
Journal | Current neurovascular research
(Curr Neurovasc Res)
Vol. 8
Issue 1
Pg. 52-63
(Feb 2011)
ISSN: 1875-5739 [Electronic] United Arab Emirates |
PMID | 21208161
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Chemical References |
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Topics |
- Animals
- Chemotaxis, Leukocyte
(genetics)
- Corpus Striatum
(blood supply, metabolism)
- Cytoprotection
(genetics)
- Disease Models, Animal
- Infarction, Middle Cerebral Artery
(genetics, metabolism, pathology)
- Mannose-Binding Lectin
(deficiency, genetics, physiology)
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Mice, Transgenic
- Neutrophils
(metabolism, pathology)
- Reperfusion Injury
(genetics, metabolism, pathology)
- Signal Transduction
(genetics)
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