p(HGNC:SELP)
Furthermore, haem-induced release of P-selectin and VWF is mediated by TLR4 and NFkB signalling. PubMed:25307023
Heme activates endothelial cells inducing the expression of the adhesion molecules ICAM-1 (intercellular adhesion molecule 1), VCAM-1 (vascular cell adhesion molecule 1), E-selectin, Pselectin, and von Willebrand factor (VWF; Wagener et al., 1997; Belcher et al., 2014) and causes neutrophil migration (GraçaSouza et al., 2002; Porto et al., 2007). PubMed:24904418
In endothelial cells, heme induces TLR4-dependent degranulation of Weibel–Palade bodies and P-selectins and VWF release. PubMed:24904418
For example, haem stimulates expression of P-selectin and von Willebrand Factor (VWF) ‘strings’ on endothelial cells in vitro and on the vessel walls of both normal and SCD mice (Belcher et al, 2014). PubMed:25307023
Monocyte–platelet interactions are believed to be predominantly mediated by surface P-selectin/integrins and their receptors, and it was suggested that monocyte-platelet aggregates are a marker of platelet activation as well as a pathway for the regulation of monocyte and platelet function [17]. PubMed:29929138
In contrast to platelet lysis, platelet activation is clearly seen, based on both the higher expression of CD62P (Fig. 3B) and increased coaggregation with white blood cells. PubMed:29929138
Surface accumulation of MAC may be at least partially responsible for the activated platelet phenotype seen in patients with primary Cys89Tyr CD59 mutation, as manifested both by increased CD62P expression and monocyte-platelet aggregates. PubMed:29929138
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
Interaction between monocytes and platelets was suggested to be via p selection [17], which was shown here to be much higher in patients with primary Cys89Tyr mutation in CD59. PubMed:29929138
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
Monocyte–platelet interactions are believed to be predominantly mediated by surface P-selectin/integrins and their receptors, and it was suggested that monocyte-platelet aggregates are a marker of platelet activation as well as a pathway for the regulation of monocyte and platelet function [17]. PubMed:29929138
In contrast to platelet lysis, platelet activation is clearly seen, based on both the higher expression of CD62P (Fig. 3B) and increased coaggregation with white blood cells. PubMed:29929138
Surface accumulation of MAC may be at least partially responsible for the activated platelet phenotype seen in patients with primary Cys89Tyr CD59 mutation, as manifested both by increased CD62P expression and monocyte-platelet aggregates. PubMed:29929138
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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.