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Shear stress augments the enhanced adhesive phenotype of cells expressing the Pro33 isoform of integrin β 3
Author(s) -
Vijayan K.Vinod,
Huang Trevor C.,
Liu Yan,
Bernardo Aubrey,
Dong Jing-Fei,
Goldschmidt-Clermont Pascal J.,
Alevriadou B.Rita,
Bray Paul F.
Publication year - 2003
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(03)00170-4
Subject(s) - fibronectin , integrin , shear stress , chemistry , cryoprecipitate , extracellular matrix , von willebrand factor , phenotype , adhesion , fibrinogen , adhesive , gene isoform , cell adhesion , microbiology and biotechnology , biophysics , platelet , materials science , immunology , biology , biochemistry , composite material , cell , gene , organic chemistry , layer (electronics)
Adhesion of platelets to the exposed extracellular matrix proteins at sites of vascular injury is partly regulated by the local fluid shear stress. Because the Leu33Pro (Pl A ) polymorphism of integrin β 3 confers only a modest increase in adhesion under static conditions, we used CHO and 293 cells expressing the Leu33 or Pro33 isoform of β 3 in flow chamber experiments to test whether shear forces would alter the Pl A adhesive phenotype. We found that shear force augmented the Pro33‐mediated enhanced adhesion to fibrinogen. This Pro33‐dependent enhancement was aspirin‐sensitive and was also observed on immobilized von Willebrand factor and cryoprecipitate, but not fibronectin. Thus, shear stress enhances the adhesive phenotype of the Pro33 cells to multiple physiologic substrates.