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

D. Inderbitzin, G. Beldi, I. Avital, G. Vinci, D. Candinas

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)142-147
Number of pages6
JournalEuropean Surgical Research
Volume36
Issue number3
DOIs
StatePublished - 26 May 2004
Externally publishedYes

Keywords

  • C1 inhibitor
  • Complement
  • Endothelial disruption
  • Ischemia-reperfusion injury
  • Permeability index
  • Transgenic mouse

Fingerprint

Dive into the research topics of 'Local and remote ischemia-reperfusion injury is mitigated in mice overexpressing human C1 inhibitor'. Together they form a unique fingerprint.

Cite this