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Leukocyte adhesion to cold‐preserved rat endothelial cells: Role of actin disassembly and ICAM‐1
Author(s) -
Topp Stefan A.,
Upadhya Gundumi A.,
Strasberg Steven M.
Publication year - 2003
Publication title -
liver transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1527-6465
DOI - 10.1016/j.lts.2003.09.008
Subject(s) - icam 1 , phalloidin , adhesion , actin , intercellular adhesion molecule 1 , microbiology and biotechnology , cell adhesion , intercellular adhesion molecule , cell adhesion molecule , biology , chemistry , cytoskeleton , cell , biochemistry , organic chemistry
Leukocyte adhesion on reperfusion is a critical component of cold preservation injury, and involves increased intercellular adhesion molecule 1 (ICAM‐1) expression on sinusoidal endothelial cells (SEC). This study determined whether ICAM‐1 expression occurs during cold preservation and whether actin disassembly is necessary for ICAM‐1 expression and leukocyte adhesion. ICAM‐1 expression was measured in isolated rat SEC during 8 hours of cold preservation by immunofluorescence techniques. Leukocyte adhesion to cold‐preserved SEC was measured in an assay using fluorescently labeled leukocytes. The calpain inhibitors N‐acetyl‐leu‐leu‐norleucinal/N‐acetyl‐leu‐leu‐methioninal and the actin stabilizer phalloidin were added in some studies to prevent actin disassembly. Cold‐exposed SEC showed a rapid increase of surface ICAM‐1 expression, reaching maximum values in 1 hour. Studies in permeabilized cells suggested that ICAM‐1 moved from a perinuclear location to the cell surface. Actin stabilization had no effect on the time‐dependent increase in ICAM‐1 expression, but seemed to affect the distribution of ICAM‐1 on the cell surface. Leukocyte adhesion to SEC correlated with ICAM‐1 expression and was reduced to control levels by an anti‐ICAM‐1 antibody. Although actin stabilization did not reduce ICAM‐1 expression, it did reduce leukocyte‐SEC adhesion to control values. Increased ICAM‐1 expression on cold‐preserved SEC is a direct effect of cold. It is not related to actin disassembly, although it seems that actin disassembly affects the distribution of ICAM‐1. Leukocyte adhesion to cold‐preserved SEC requires both increased ICAM‐1 and actin disassembly. Agents that inhibit actin disassembly can significantly decrease leukocyte adhesion regardless of increased ICAM‐1 expression.