Collagen-induced platelet aggregation is associated with a burst of H2O2 that acts as a second messenger by stimulating arachidonic acid metabolism and the phospholipase C pathway.
This study demonstrates that hydrogen peroxide acts as a second messenger in collagen-induced platelet activation, stimulating arachidonic acid metabolism and the phospholipase C pathway.
In this study, we investigated whether (1) collagen-induced platelet aggregation is associated with a burst of H2O2, (2) this oxidant species is involved in the activation of platelets, and (3) the pathways of platelet activation are stimulated by H2O2. Collagen-induced platelet aggregation was associated with production of H2O2, which was abolished by catalase, an enzyme that destroys H2O2. H2O2 production was not observed when ADP or thrombin were used as agonists. Catalase inhibited dose-dependently thromboxane A2 production, release of arachidonic acid from platelet membrane, and Inositol 1,4,5P3 (IP3) formation. In aspirin-treated platelets stimulated with high concentrations of collagen, catalase inhibited platelet aggregation, calcium mobilization, and IP3 production. This study suggests that collagen-induced platelet aggregation is associated with a burst of H2O2 that acts as a second messenger by stimulating the arachidonic acid metabolism and phospholipase C pathway.
Pignatelli et al. (Thu,) conducted a other in Platelet activation. Collagen and Catalase was evaluated on Platelet aggregation, H2O2 production, and pathway activation. Collagen-induced platelet aggregation is associated with a burst of H2O2 that acts as a second messenger by stimulating arachidonic acid metabolism and the phospholipase C pathway.