title: An in vitro model of warm hypoxia-reoxygenation injury in human liver endothelial cells.
abstract: BACKGROUND
  Ischemia-reperfusion or hypoxia-reoxygenation (H-R) injury adversely affects hepatic function following transplantation and major resection; the death of human sinusoidal endothelial cells (SECs) by apoptosis may play a central role in this process. Caspase-3 is an important intracellular protease in the intrinsic and extrinsic pathways of apoptosis.
  
  
  METHODS
  SECs and EAhy926 cells were exposed to warm hypoxia at 37°C, followed by reoxygenation at 37°C. Activity of caspase-3 was quantified using Western blotting and colorimetric kinase assays.
  
  
  RESULTS
  H-R caused a significant increase in caspase-3 activity compared with controls in both cell types.
  
  
  CONCLUSIONS
  Warm H-R injury causes apoptotic cell death of SECs and immortalized cells, but with differing patterns of caspase activity.
authors.affiliation: Department of Hepatobiliary Surgery and Transplantation, St. James' University Hospital, Leeds, United Kingdom. nealbanga@nhs.net
authors.forename: Neal R
authors.initials: NR
authors.lastname: Banga
authors.forename: K Raj
authors.initials: KR
authors.lastname: Prasad
authors.forename: J Lance
authors.initials: JL
authors.lastname: Burn
authors.forename: Shervanthi
authors.initials: S
authors.lastname: Homer-Vanniasinkam
authors.forename: Anne
authors.initials: A
authors.lastname: Graham
mesh_terms: D017209:Apoptosis / Q000502:physiology*; D053148:Caspase 3 / Q000378:metabolism; D002461:Cell Line, Transformed; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology*; D006358:Hot Temperature / Q000009:adverse effects; D006801:Humans; D000860:Hypoxia / Q000378:metabolism / Q000473:pathology*; D008099:Liver / Q000378:metabolism / Q000473:pathology*; D016031:Liver Transplantation; D061251:Primary Cell Culture; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology*
chemical_list: C505407:CASP3 protein, human; D053148:Caspase 3