What question did this study set out to answer?

Investigate how physiological concentrations of thrombin regulate the exposure of the factor VIII/von Willebrand factor receptor on human platelets and determine the inhibitory effects of prostacyclin.

June 1, 1982Journal of Clinical InvestigationOpen Access

Thrombin-induced exposure and prostacyclin inhibition of the receptor for factor VIII/von Willebrand factor on human platelets.

View Full Paper

Ask AI

Bookmark

Authors

TFT FujimotoThe University of Osaka SOS. OharaOkayama University JHJacek HawigerVanderbilt University

Discussion

Member takes

Implication

Experimental study uncovers thrombin-stimulated factor VIII/von Willebrand factor receptor binding and its reversal by prostacyclin in human platelets, indicating dynamic control of platelet adhesion.

Key Points

Investigate how physiological concentrations of thrombin regulate the exposure of the factor VIII/von Willebrand factor receptor on human platelets and determine the inhibitory effects of prostacyclin.
Measured binding of 125I-labeled factor VIII/von Willebrand factor to human platelets stimulated with physiological levels of thrombin (0.008–0.05 U/ml).
Evaluated binding specificity and membrane requirements using excess unlabeled ligand, monospecific antibodies, chelating agents (EDTA, EGTA), and chymotrypsin digestion.
Tested the capacity of prostacyclin (1–50 nM) and dibutyryl cyclic AMP to inhibit receptor exposure before thrombin addition or reverse ligand binding at equilibrium.
Thrombin at 0.008–0.05 U/ml induced concentration-dependent, specific binding of factor VIII/von Willebrand factor that required metabolically active platelets, divalent cations, and surface glycoproteins, with chymotrypsin stripping reducing binding by 2.5–5.0-fold.
Prostacyclin (1–50 nM) and dibutyryl cyclic AMP completely prevented receptor exposure when added 10 minutes before thrombin and reversed receptor-bound ligand when added 30 minutes after activation at equilibrium.

Cite This Study

Fujimoto et al. (1982) studied this question.

synapsesocial.com/papers/6a7104fd26a7f98052dd7489 https://doi.org/10.1172/jci110560

View Full Paper

Ask AI

Bookmark

June 1, 1982Journal of Clinical InvestigationOpen Access

Thrombin-induced exposure and prostacyclin inhibition of the receptor for factor VIII/von Willebrand factor on human platelets.

View Full Paper

Ask AI

Bookmark

Authors

TFT FujimotoThe University of Osaka SOS. OharaOkayama University JHJacek HawigerVanderbilt University

Discussion

Member takes

Implication

Key Points

Investigate how physiological concentrations of thrombin regulate the exposure of the factor VIII/von Willebrand factor receptor on human platelets and determine the inhibitory effects of prostacyclin.
Measured binding of 125I-labeled factor VIII/von Willebrand factor to human platelets stimulated with physiological levels of thrombin (0.008–0.05 U/ml).
Evaluated binding specificity and membrane requirements using excess unlabeled ligand, monospecific antibodies, chelating agents (EDTA, EGTA), and chymotrypsin digestion.
Tested the capacity of prostacyclin (1–50 nM) and dibutyryl cyclic AMP to inhibit receptor exposure before thrombin addition or reverse ligand binding at equilibrium.
Thrombin at 0.008–0.05 U/ml induced concentration-dependent, specific binding of factor VIII/von Willebrand factor that required metabolically active platelets, divalent cations, and surface glycoproteins, with chymotrypsin stripping reducing binding by 2.5–5.0-fold.
Prostacyclin (1–50 nM) and dibutyryl cyclic AMP completely prevented receptor exposure when added 10 minutes before thrombin and reversed receptor-bound ligand when added 30 minutes after activation at equilibrium.

Cite This Study

Fujimoto et al. (1982) studied this question.

synapsesocial.com/papers/6a7104fd26a7f98052dd7489 https://doi.org/10.1172/jci110560

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

View Full Paper

Ask AI

Bookmark