First Author | Inderbitzin D | Year | 2004 |
Journal | Eur Surg Res | Volume | 36 |
Issue | 3 | Pages | 142-7 |
PubMed ID | 15178902 | Mgi Jnum | J:127680 |
Mgi Id | MGI:3764602 | Doi | 10.1159/000077255 |
Citation | Inderbitzin D, et al. (2004) Local and remote ischemia-reperfusion injury is mitigated in mice overexpressing human C1 inhibitor. Eur Surg Res 36(3):142-7 |
abstractText | Activation of the classical complement pathway is crucially involved in complement-mediated endothelial cell damage in ischemia-reperfusion injury. C1 inhibitor is the only known physiological inhibitor of classical complement pathway activation. Transgenic mice overexpressing human C1 inhibitor were used in a surgical lower torso and a liver ischemia-reperfusion model. Organ-specific endothelial disruption was determined by 125I-tagged albumin extravasation. In the lower torso ischemia-reperfusion model, transgenic mice overexpressing the C1 inhibitor were protected in the muscle and the lungs from endothelial cell damage. In the liver ischemia-reperfusion model, endothelial cell integrity was preserved in transgenic animals in the liver, the gut and the lungs. Our data indicate that inhibiting complement activation by a transgenic approach is effective in protection against ischemia-reperfusion injury. |