Erythrocyte and platelet proteomics in hematological disorders

Abstract

Erythrocytes undergo ineffective erythropoesis, hemolysis, and premature eryptosis in sickle cell disease and thalassemia. Abnormal hemoglobin variants associated with hemoglobinopathy lead to vesiculation, membrane instability, and loss of membrane asymmetry with exposal of phosphatidylserine. This potentiates thrombin generation resulting in activation of the coagulation cascade responsible for subclinical phenotypes. Platelet activation also results in the release of microparticles, which express and transfer functional receptors from platelet membrane, playing key roles in vascular reactivity and activation of intracellular signaling pathways. Over the last decade, proteomics had proven to be an important field of research in studies of blood and blood diseases. Blood cells and its fluidic components have been proven to be easy systems for studying differential expressions of proteins in hematological diseases encompassing hemoglobinopathies, different types of anemias, myeloproliferative disorders, and coagulopathies. Proteomic studies of erythrocytes and platelets reported from several groups have highlighted various factors that intersect the signaling networks in these anucleate systems. In this review, we have elaborated on the current scenario of anucleate blood cell proteomes in normal and diseased individuals and the cross-talk between the two major constituent cell types of circulating blood.

Redox Proteomics and Platelet Activation: Understanding the Redox Proteome to Improve Platelet Quality for Transfusion

“…Nevertheless, for more than 20 years ROS have not only been shown to be deleterious, but also to actively regulate platelet signaling and activation [28]. The results from recent redox proteomic approaches, together with classical approaches, highlight the importance of a complex redox cellular system that can influence the resting platelet state [29]. PITs could interfere with this state due to their intrinsic nature.…”

Development of a label‒free nanolc/ms/ms assay for monitoring the changes in the proteomic landscape of thrombin‒activated human platelets

“…PRP were subjected to the whole platelets purification as described previously by other research groups. [30][31][32][33][34][35] Then, platelets were pelleted at 750xg for 10min and twice washed with the Tyrode's Buffer containing 134mM NaCl, 12mM NaHCO 3 , 2.9mM KCl, 0.34mM Na 2 HPO 4 , 1mM MgCl 2 , and 10mM Hepes (pH 7.4). Platelet count Development of a label-free nanolc/ms/ms assay for monitoring the changes in the proteomic landscape of thrombin-activated human platelets 234 Copyright: ©2018 Gonzalez et al Citation: Gonzalez J, Babinska A, Ewul ELV, et al Development of a label-free nanolc/ms/ms assay for monitoring the changes in the proteomic landscape of thrombin-activated human platelets.…”

The Clinical Utility of Circulating Microparticles’ Measurement in Heart Failure Patients

“…Indeed, erythrocytes actively shed phospholipid-bound MPs [54]. MPs originating from erythrocytes are naturally produced in vivo during normal aging processes or they have associated with a variety of pathophysiological conditions including hematology diseases (hemolysis, sickle cell disease and thalassemia), chronic kidney disease (IgA nephropathy), uremia, stroke, acute infections, sepsis, trauma, thrombosis/embolia, allograft dysfunction [55][56][57][58][59][60]. Therefore, erythrocytes-derived MPs may secrete ex vivo during cold storage of RBCs [61].…”

“…It has been defined that lipopolysaccharides, immune complexes, complement components, abnormal hemoglobin variants might lead to vesiculation, membrane instability, and loss of membrane asymmetry of erythrocytes with exposal of phosphatidylserine [55,56]. This potentiates thrombin generation resulting in activation of the coagulation cascade via the tenase and prothrombinase complexes responsible for subclinical phenotypes and increase of the atherothrombotic and CV risk [62].…”