Key result
Thrombomodulin activates NOS3 via a tyrosine kinase pathway to induce nitric oxide and calcium signals.
Why the study?
The mechanisms by which endothelial thrombomodulin transduces signals to activate endothelial nitric-oxide synthase and modulate G protein-coupled receptor signaling were unclear.
Population
Cultured human umbilical vein endothelial cells
Comparison
Thrombin vs mutant thrombin binding thrombomodulin without PAR-1 activity
Design
Preclinical cellular signaling study
Authors
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Hypothesis-generating for thrombomodulin in vascular disease; leaves open translation to human thrombosis therapies.
This study demonstrates that the cell surface thrombomodulin receptor mediates an outside-in signal to activate NOS3 through a tyrosine kinase-dependent pathway, potentially contributing to its function in thrombosis, inflammation, and atherosclerosis.
David‐Dufilho et al. (2005) studied this question. Thrombin and mutant thrombin was evaluated on Nitric oxide release and Ca2+ signals. Thrombomodulin transduces an outside-in signal to activate NOS3 through a tyrosine kinase-dependent pathway, inducing Ca2+ signals and nitric oxide synthesis.
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