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Differential regulation of transendothelial migration of THP‐1 cells by ICAM‐1/LFA‐1 and VCAM‐1/VLA‐4
Author(s) -
Ronald John A.,
Ionescu Carmen V.,
Rogers Kem A.,
Sandig Martin
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.70.4.601
Subject(s) - vcam 1 , biology , microbiology and biotechnology , filopodia , cdc42 , icam 1 , intercellular adhesion molecule 1 , cell adhesion molecule , pseudopodia , cell adhesion , thp1 cell line , motility , blockade , adhesion , cell culture , receptor , signal transduction , cell , actin , biochemistry , chemistry , genetics , organic chemistry
The adhesion molecules intercellular adhesion molecule 1 (ICAM‐1) and vascular cell adhesion molecule 1 (VCAM‐1) expressed in atherogenic lesions are thought to regulate monocyte diapedesis. To better understand their specific roles we used function‐blocking antibodies and examined in a culture model the morphology, motility, and diapedesis of THP‐1 cells interacting with human coronary artery endothelial cells. The number of motile THP‐1 cells was reduced only when VCAM‐1 or both ICAM‐1 and VCAM‐1 were blocked. Blockade of ICAM‐1 and VCAM‐1, either separately or together, reduced to the same degree the distance that THP‐1 cells traveled. Diapedesis was reduced only during the simultaneous blockade of both adhesion molecules. Blockade of either ICAM‐1 or VCAM‐1 inhibited pseudopodia formation, but ICAM‐1 blockade induced the formation of filopodia. We suggest that the interactions of endothelial ICAM‐1 and VCAM‐1 with their ligands differentially regulate distinct steps of diapedesis by modulating the ratio of active and inactive forms of small GTPases such as Rho, Rac, and Cdc42.