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Publication : Local and remote ischemia-reperfusion injury is mitigated in mice overexpressing human C1 inhibitor.

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.
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