Apical topography and modulation of ICAM-1 expression on activated endothelium.

摘要: Abstract Leukocyte-endothelium interactions and general inflammatory responses are contributed by the regulated expression of intercellular adhesion molecule-1 (ICAM-1) on endothelium. It is now shown confocal fluorescence microscopy immunogold transmission electron that ICAM-1 was exclusively localized apical (luminal) membrane cytokine-activated human umbilical vein endothelial cells. In contrast, other cell adhesion-promoting molecules, including beta 1 integrins, were expressed basolateral membrane, under same experimental conditions. Kinetic binding studies a 125I-labeled monoclonal antibody to revealed approximately 8% endothelium internalized in both coated non-coated vesicles at 37 degrees C, with t1/2 18 min rate 3200 molecules/minute. This internalization pathway directly dependent upon level surface. Genetically engineered transfectants, expressing 10-fold higher receptor density than activated endothelium, 18% 75,000 molecules/minute 22 min. These findings suggest combined polarized topography trafficking may regulate ICAM-1-dependent site vascular injury activation.