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Shear stress‐induced shedding of soluble intercellular adhesion molecule‐1 from saphenous vein endothelium
Author(s) -
Sultan Sabena,
Gosling Martin,
Nagase Hideaki,
Powell Janet T
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(04)00337-0
Subject(s) - intercellular adhesion molecule 1 , icam 1 , downregulation and upregulation , endothelium , matrix metalloproteinase , chemistry , intracellular , medicine , microbiology and biotechnology , biology , biochemistry , gene
Within 6 h, shear stress upregulated intercellular adhesion molecule‐1 (ICAM‐1) (two‐ to four‐fold, P <0.001) and induced matrix metalloproteinase‐2 (MMP‐2) in cultured human saphenous vein endothelial cells. By 8 h endothelial ICAM‐1 levels returned to baseline, with concomitant increase in soluble ICAM‐1 (sICAM‐1) ( P <0.001) and MMP‐9 had been induced. Inclusion of a hydroxamate metalloproteinase inhibitor partially reversed the effects on ICAM‐1 and sICAM‐1 at 8 h, whereas TIMP‐1, ‐2 or ‐3 had no effect. MMP‐9, but not MMP‐2, co‐immunoprecipitated with ICAM‐1. sICAM‐1 was processed distal to Arg441, indicating that MMP‐9, docking to ICAM‐1, contributes to sICAM‐1 shedding and attenuation of the shear stress‐induced upregulation of ICAM‐1.