Shear stress augments the enhanced adhesive phenotype of cells expressing the Pro33 isoform of integrin β3

FEBS Letters

Liu, Yan³  Bray, Paul F.³  Bernardo, Aubrey³  Vijayan, K.Vinod³  Alevriadou, B.Rita²  Dong, Jing-Fei³  Goldschmidt-Clermont, Pascal J.¹  Huang, Trevor C.² 

[1] Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA;Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA;Department of Medicine, Baylor College of Medicine, One Baylor Plaza, BCM 286, N1319, Houston, TX 77030, USA

关键词: β3 integrin;    PlA polymorphism;    Shear stress;    ECM;    extracellular matrix;    vWF;    von Willebrand factor;    ASA;    acetylsalicylic acid;    COX;    cyclooxygenase;   

DOI  :  10.1016/S0014-5793(03)00170-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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 β₃ confers only a modest increase in adhesion under static conditions, we used CHO and 293 cells expressing the Leu33 or Pro33 isoform of β₃ 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.

【 授权许可】

Unknown