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- W2014164920 endingPage "164" @default.
- W2014164920 startingPage "141" @default.
- W2014164920 abstract "Cellular interactions play a key role in diverse biological processes within the cardiovascular system. Targeting of leukocytes to sites of inflammation is viewed as a multistage process of sequential involvement of distinct adhesion molecules on the leukocyte and endothelial cell (EC) surface that is dictated by the local fluid dynamic environment. For neutrophils, the initial contact and rolling along the vessel wall are mediated primarily by selectins. Subsequent firm adhesion requires activation of neutrophil β2 integrins and binding to their ligand ICAM-1 on the EC surface. The final step of this cascade of events includes neutrophil transmigration to extravascular tissue space. The neutrophil model of emigration in inflammation has been extended and refined to account for monocyte and T cell interactions with ECs. Platelet adhesion to thrombogenic surfaces (i.e. immobilized von Willebrand factor) under flow follows the general principles of leukocyte extravasation. More specifically, platelet glycoprotein (GP) Ibα appears to mediate an initial selectin-like tethering platelet–vWf interaction, followed by αIIββ3 integrin activation and firm adhesion. Some of the signaling mechanisms associated with cellular interactions in inflammatory and thrombotic processes are discussed. These basic principles are also discussed in the context of tissue engineering research." @default.
- W2014164920 created "2016-06-24" @default.
- W2014164920 creator A5036132457 @default.
- W2014164920 creator A5041184949 @default.
- W2014164920 creator A5049898092 @default.
- W2014164920 date "1998-08-01" @default.
- W2014164920 modified "2023-10-03" @default.
- W2014164920 title "Biomechanics of cell interactions in shear fields" @default.
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