TY - JOUR
T1 - Expression of complement-regulatory proteins in normal and UW-preserved human liver
AU - Scoazec, Jean Yves
AU - Delautier, Danièle
AU - Moreau, Alain
AU - Durand, François
AU - Degott, Claude
AU - Benhamou, Jean Pierre
AU - Belghiti, Jacques
AU - Feldmann, Gérard
N1 - Funding Information:
Supported by a grant from the Ministore de la Recherche et de la Technologie (no. 92CO305).
PY - 1994/1/1
Y1 - 1994/1/1
N2 - Background/Aims: 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.
AB - Background/Aims: 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.
UR - http://www.scopus.com/inward/record.url?scp=0027936127&partnerID=8YFLogxK
U2 - 10.1016/0016-5085(94)90178-3
DO - 10.1016/0016-5085(94)90178-3
M3 - Article
C2 - 7518785
AN - SCOPUS:0027936127
SN - 0016-5085
VL - 107
SP - 505
EP - 516
JO - Gastroenterology
JF - Gastroenterology
IS - 2
ER -