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ICAM‐1 diffusion enhances leukocyte adhesion under flow conditions
Author(s) -
Kucik Dennis F,
Wu Xing,
Gupta Kiran
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a126-d
Subject(s) - integrin , microbiology and biotechnology , adhesion , icam 1 , cell adhesion , cell adhesion molecule , intercellular adhesion molecule 1 , cytoskeleton , chemistry , receptor , biophysics , biology , cell , biochemistry , organic chemistry
Integrins on leukocytes modulate adhesiveness both by modulating affinity of the individual receptor and by rearranging the receptors by diffusion. Diffusion of β 2 integrins in the plane of the leukocyte membrane is thought to be pro‐adhesive for two reasons: movement of the integrins increases the kinetics of ligand binding, and the motion eventually leads to clustering. Connections between ICAM‐1 (the β 2 integrin ligand on endothelial cells) and the cytoskeleton are regulated, but whether movement of ICAM‐1 in the endothelial cell membrane has an effect on adhesion has not been tested. To test this, we expressed wild type ICAM‐1 and a GPI‐linked ICAM‐1 construct in 293 cells. Single Particle Tracking demonstrated that the wild type ICAM‐1 was immobilized by the cytoskeleton, while the GPI‐linked form diffused. We then compared adhesion of WEHI monocytic cells to 293‐cell monolayers expressing each form of ICAM‐1. Adhesion (via β 2 integrins) of monocytic cells under flow was greater on 293 cells expressing GPI‐linked ICAM‐1. Immunofluorescence demonstrated no significant difference in clustering of the two forms of ICAM‐1. These experiments suggest that lateral mobility of ICAM‐1 can contribute to leukocyte adhesion to endothelium under flow, independent of ICAM‐1 clustering.