References
Query Results -- Details
MGI Accession ID: MGI:3718959
J Number: J:123658
Other Accession IDs:
Title: Complement component C3 mediates inflammatory injury following focal cerebral ischemia.
Authors: Mocco J; Mack WJ; Ducruet AF; Sosunov SA; Sughrue ME; Hassid BG; Nair MN; Laufer I; Komotar RJ; Claire M; Holland H; Pinsky DJ; Connolly ES Jr
Journal: Circ Res
Volume: 99
Issue: 2
Date: 2006 Jul 21
Year: 2006
Pages: 209-17
Review Status: Peer Reviewed
Abstract:
The complement cascade has been implicated in ischemia/reperfusion injury, and recent studies have shown that complement inhibition is a promising treatment option for acute stroke. The development of clinically useful therapies has been hindered, however, by insufficient understanding of which complement subcomponents contribute to post-ischemic injury. To address this issue, we subjected mice deficient in selected complement proteins (C1q, C3, C5) to transient focal cerebral ischemia. Of the strains investigated, only C3-/- mice were protected, as demonstrated by 34% reductions in both infarct volume (P<0.01) and neurological deficit score (P<0.05). C3-deficient mice also manifested decreased granulocyte infiltration (P<0.02) and reduced oxidative stress (P<0.05). Finally, administration of a C3a-receptor antagonist resulted in commensurate neurological improvement and stroke volume reduction (P<0.05). Together, these results establish C3 activation as the key constituent in complement-related inflammatory tissue injury following stroke and suggest a C3a anaphylatoxin-mediated mechanism.
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