title: Expression of complement-regulatory proteins in normal and UW-preserved human liver.
abstract: OBJECTIVE
  Somatic cells are protected against complement-mediated injury by specialized membrane proteins, known as complement-regulatory proteins (CRP). The knowledge of the pattern of CRP expression in the liver is important to evaluate the role of complement-mediated injury in graft rejection.
  
  
  METHODS
  We determined the distribution of four main CRP: membrane cofactor protein (MCP), decay accelerating factor (DAF), protectin, and complement receptor 1 (CR1) in 30 histologically normal livers, 13 samples from University of Wisconsin cold-storage solution (UW)-preserved tissue and 17 postoperative biopsies of UW-preserved allografts.
  
  
  RESULTS
  In normal liver, hepatocytes expressed only MCP. Bile duct cells were reactive for MCP and protectin. Sinusoidal endothelial cells expressed MCP and protectin but displayed no or faint expression of DAF. Endothelial cells of portal vessels and centrilobular veins expressed high levels of DAF, MCP, and protectin. No expression of CR1 was observed. No change in CRP expression was usually detected after UW preservation, except for protectin, induced on hepatocytes in 9 samples of UW-preserved liver tissue and in 9 allografts.
  
  
  CONCLUSIONS
  Hepatocytes and sinusoidal endothelial cells, which have a defective expression of CRP, might be at risk for complement-mediated injury. However, this risk is not aggravated after UW preservation.
authors.affiliation: Laboratoire de Biologie Cellulaire and Unité INSERM U327, Faculté de Médecine Xavier Bichat, Paris, France.
authors.forename: J Y
authors.initials: JY
authors.lastname: Scoazec
authors.forename: D
authors.initials: D
authors.lastname: Delautier
authors.forename: A
authors.initials: A
authors.lastname: Moreau
authors.forename: F
authors.initials: F
authors.lastname: Durand
authors.forename: C
authors.initials: C
authors.lastname: Degott
authors.forename: J P
authors.initials: JP
authors.lastname: Benhamou
authors.forename: J
authors.initials: J
authors.lastname: Belghiti
authors.forename: G
authors.initials: G
authors.lastname: Feldmann
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000328:Adult; D000493:Allopurinol / Q000494:pharmacology; D015703:Antigens, CD / Q000378:metabolism*; D018958:CD55 Antigens; D018957:CD59 Antigens; D003169:Complement Inactivator Proteins / Q000378:metabolism*; D003165:Complement System Proteins / Q000378:metabolism*; D005260:Female; D005978:Glutathione / Q000494:pharmacology; D006801:Humans; D007328:Insulin / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D016031:Liver Transplantation; D008297:Male; D051916:Membrane Cofactor Protein; D008562:Membrane Glycoproteins / Q000378:metabolism*; D008875:Middle Aged; D009926:Organ Preservation; D019188:Organ Preservation Solutions; D011887:Raffinose / Q000494:pharmacology; D017463:Receptors, Complement 3b / Q000378:metabolism*
chemical_list: D015703:Antigens, CD; C497857:CD46 protein, human; D018958:CD55 Antigens; D018957:CD59 Antigens; D003169:Complement Inactivator Proteins; D007328:Insulin; D051916:Membrane Cofactor Protein; D008562:Membrane Glycoproteins; D019188:Organ Preservation Solutions; D017463:Receptors, Complement 3b; C055206:University of Wisconsin-lactobionate solution; D000493:Allopurinol; D003165:Complement System Proteins; D005978:Glutathione; D000241:Adenosine; D011887:Raffinose