bp(MESH:"Platelet Aggregation")
NO inhibits platelet aggregation mediated by guanylate cyclase activation with a subsequent rise in cGMP (Faint et al, 1991). PubMed:25307023
Platelet deposition and adhesion at sites of subintimal injury are increased by free haemoglobin or inhibition of NO production; this effect can be prevented by infusions of L-arginine, the precursor of NO (Olsen et al, 1996). PubMed:25307023
Platelet deposition and adhesion at sites of subintimal injury are increased by free haemoglobin or inhibition of NO production; this effect can be prevented by infusions of L-arginine, the precursor of NO (Olsen et al, 1996). PubMed:25307023
Both processes decrease the availability of NO, which normally maintains smooth muscle cell relaxation, inhibits platelet activation and aggregation, and has anti-inflammatory effects on the endothelium. PubMed:29929138
Platelet deposition and adhesion at sites of subintimal injury are increased by free haemoglobin or inhibition of NO production; this effect can be prevented by infusions of L-arginine, the precursor of NO (Olsen et al, 1996). PubMed:25307023
Moreover, in vitro studies have demonstrated that heme binds to human platelets and induces platelet activation and aggregation [37–39]. PubMed:26875449
RBCs can modulate platelet reactivity directly through either chemical signaling or adhesive RBC-platelet interactions. RBCs promote platelet aggregation and degranulation by releasing ATP and ADP under low pO2, low pH and in response to mechanical deformation [27, 28]. PubMed:28458720
When RBCs are damaged by high shear in continuous flow ventricular assist devices, free hemoglobin induces platelet aggregation, contributing to high risk of thrombotic complications [33]. PubMed:28458720
Extracellular hemoglobin sequesters NO and thus promotes activation of endothelial cells and adhesion/aggregation of platelets [64]. PubMed:28458720
In patients with SCD (Wun et al, 1998) and b-thalassaemia (Ruf et al, 1997), flow cytometry demonstrates the presence of an increased fraction of platelets expressing P-selectin, a platelet membrane receptor that mediates platelet–endothelial interactions. PubMed:25307023
In addition, reduced NO bioavailability induces platelet activation and aggregation, leading to thrombosis in a mouse model of intravascular haemolysis (Hu et al, 2010). PubMed:25307023
In addition, reduced NO bioavailability induces platelet activation and aggregation, leading to thrombosis in a mouse model of intravascular haemolysis (Hu et al, 2010). PubMed:25307023
When RBCs are damaged by high shear in continuous flow ventricular assist devices, free hemoglobin induces platelet aggregation, contributing to high risk of thrombotic complications [33]. PubMed:28458720
In patients with SCD (Wun et al, 1998) and b-thalassaemia (Ruf et al, 1997), flow cytometry demonstrates the presence of an increased fraction of platelets expressing P-selectin, a platelet membrane receptor that mediates platelet–endothelial interactions. PubMed:25307023
BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.
If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.