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  • receptor
  • While confirming that both thrombin and neutrophil elastase proteolyse GPV, we show that neutrophil cathepsin G, thrombin receptor activating peptide (TRAP), and a combination of ADP and epinephrine can each result in a decrease in the platelet surface expression of GPV by a nonproteolytic mechanism: a cytoskeletal-mediated redistribution of platelet surface GPV to the surface-connected canalicular system (SCCS). (umassmed.edu)
  • The experiments with TRAP showed that activation of the seven-transmembrane domain thrombin receptor can result in translocation of GPIb, GPIX, and GPV to the SCCS independently of the GPIb-mediated pathway of thrombin-induced platelet activation. (umassmed.edu)
  • agonists
  • The cytoskeletal-mediated redistribution of GPV occurred in a whole blood milieu and at physiologic temperatures (37 degrees C) and extracellular calcium concentrations (2 mmol/L). This study also defines the diverse effects on GPV, GPIb, and GPIX of multiple important platelet agonists. (umassmed.edu)
  • Elastase proteolysed platelet surface GPIb alpha and GPV, but, unlike the other agonists tested, neither proteolysed nor redistributed platelet surface GPIX. (umassmed.edu)
  • total platelet
  • First, flow cytometric studies showed that cathepsin G, TRAP, and ADP/epinephrine decreased the platelet surface expression of GPV without changing the total platelet content of GPV. (umassmed.edu)
  • surface
  • The platelet surface expression of glycoprotein V is regulated by two " by Alan D. Michelson, Stephen E. Benoit et al. (umassmed.edu)
  • Four independent lines of evidence documented the nonproteolytic nature of this decrease in the platelet surface expression of GPV. (umassmed.edu)
  • Second, immunoelectron microscopy directly demonstrated translocation of GPV from the platelet surface to the SCCS. (umassmed.edu)
  • Third, the cathepsin G-, TRAP-, and ADP/epinephrine-induced decreases in platelet surface GPV were fully reversible. (umassmed.edu)
  • Fourth, cytochalasin B, an inhibitor of actin polymerization, completely inhibited the cathepsin G-, TRAP-, and ADP/epinephrine-induced decreases in platelet surface GPV. (umassmed.edu)
  • Second, triple labeling flow cytometric experiments showed that, on each individual platelet, the ADP/epinephrine-induced decrease and subsequent return of the platelet surface expression of GPV occurred simultaneously with the decrease and subsequent return of the platelet surface expression of GPIb. (umassmed.edu)
  • The underlying biochemical defect in BSS is the absence or decreased expression of the GPIb/IX/V complex on the surface of the platelets. (medscape.com)