| http://purl.uniprot.org/citations/17082645 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17082645 | http://www.w3.org/2000/01/rdf-schema#comment | "The mechanisms that contribute to inflammatory damage following ischemic stroke are poorly characterized, but studies indicate a role for both complement and P-selectin. In this study, we show that compared with wild-type mice, C3-deficient mice showed significant improvement in survival, neurological deficit, and infarct size at 24 h after middle cerebral artery occlusion and reperfusion. Furthermore, P-selectin protein expression was undetectable in the cerebral microvasculature of C3-deficient mice following reperfusion, and there was reduced neutrophil influx, reduced microthrombus formation, and increased blood flow postreperfusion in C3-deficient mice. We further investigated the use of a novel complement inhibitory protein in a therapeutic paradigm. Complement receptor 2 (CR2)-Crry inhibits complement activation at the C3 stage and targets to sites of complement activation. Treatment of normal mice with CR2-Crry at 30 min postreperfusion resulted in a similar level of protection to that seen in C3-deficient mice in all of the above-measured parameters. The data demonstrate an important role for complement in cerebrovascular thrombosis, inflammation, and injury following ischemic stroke. P-selectin expression in the cerebrovasculature, which is also implicated in cerebral ischemia and reperfusion injury, was shown to be distal to and dependent on complement activation. Data also show that a CR2-targeted approach of complement inhibition provides appropriate bioavailability in cerebral injury to enable complement inhibition at a dose that does not significantly affect systemic levels of serum complement activity, a potential benefit for stroke patients where immunosuppression would be undesirable due to significantly increased susceptibility to lung infection."xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.177.10.7266"xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/author | "Song H."xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/author | "Yu J."xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/author | "Zhu H."xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/author | "Atkinson C."xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/author | "Tomlinson S."xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/author | "Qiao F."xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/author | "Kindy M.S."xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/author | "Varela J.C."xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/pages | "7266-7274"xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/title | "Complement-dependent P-selectin expression and injury following ischemic stroke."xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://purl.uniprot.org/core/volume | "177"xsd:string |
| http://purl.uniprot.org/citations/17082645 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17082645 |
| http://purl.uniprot.org/citations/17082645 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/17082645 |
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| http://purl.uniprot.org/uniprot/#_A0A0A6YY75-mappedCitation-17082645 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17082645 |