AI Article Synopsis
- The adhesion of platelets at vascular injury sites is influenced by fluid shear stress, which can affect the behavior of specific integrin beta(3) variations.
- In experiments using different cell types, shear force was found to increase the adhesion of cells expressing the Pro33 form of integrin beta(3) more than the Leu33 form.
- This stronger adhesion under shear stress was sensitive to aspirin and was noted with certain proteins like fibrinogen and von Willebrand factor, but not with fibronectin.
Article Abstract
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 beta(3) confers only a modest increase in adhesion under static conditions, we used CHO and 293 cells expressing the Leu33 or Pro33 isoform of beta(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.
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| http://dx.doi.org/10.1016/s0014-5793(03)00170-4 | DOI Listing |
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