| First Author | Mocco J | Year | 2006 |
| Journal | Circ Res | Volume | 99 |
| Issue | 2 | Pages | 209-17 |
| PubMed ID | 16778128 | Mgi Jnum | J:123658 |
| Mgi Id | MGI:3718959 | Doi | 10.1161/01.RES.0000232544.90675.42 |
| Citation | Mocco J, et al. (2006) Complement component C3 mediates inflammatory injury following focal cerebral ischemia. Circ Res 99(2):209-17 |
| abstractText | 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. |
