Abstract
Blood banks use pathogen inactivation (PI) technologies to increase the safety of platelet concentrates (PCs). The characteristics of PI-treated PCs slightly differ from those of untreated PCs, but the underlying reasons are not well understood. One possible cause is the generation of oxidative stress during the PI process. This is of great interest since reactive oxygen species (ROS) act as second messengers in platelet functions. Furthermore, there are links between protein oxidation and phosphorylation, another mechanism that is critical for cell regulation. Current research efforts focus on understanding the underlying mechanisms and identifying new target proteins. Proteomics technologies represent powerful tools for investigating signaling pathways involving ROS and post-translational modifications such as phosphorylation, while quantitative techniques enable the comparison of the platelet resting state versus the stimulated state. In particular, redox cysteine is a key player in platelet activation upon stimulation by different agonists. This review highlights the experiments that have provided insights into the roles of ROS in platelet function and the implications for platelet transfusion, and potentially in diseases such as inflammation and platelet hyperactivity. The review also describes the implication of redox mechanism in platelet storage considerations.
Highlights
Platelets are anucleate cells that are involved in hemostasis and in many inflammatory processes [1,2]
While protein carbonylation is generally considered to be deleterious and associated with diseases [47], it might well be one of the final steps of the oxidation chain caused by reactive oxygen species (ROS) in platelet activation that participates in redox signaling [54]
ROS generation is significantly decreased by inhibiting focal adhesion tyrosine kinase in the GPIbα–PAR4 downstream cascade [59], while the main receptor, PAR-1, which has a high affinity for thrombin, seems to activate platelets via ROS-independent pathways
Summary
Platelets are anucleate cells that are involved in hemostasis and in many inflammatory processes [1,2]. Activated platelets form stress is one possible cause of the proteins, functional forming changes in platelets that are crosslinks Oxidative via fibrinogen bridges between αIIbβ the thrombus (6).observed in vitro after PIT treatment [19,20]. PCs. Differences in data collection methods make it difficult to compare studies, so the clinical relevance of PITs in platelet function remains unclear in terms of CCI and bleeding time [17,18]. Redox proteomics provide tools that can describe these phenomena and that can be used to monitor both reversible and irreversible modifications of the protein oxidation state that play roles in biological structures and cell functionality [33]. Discussions are opened on the actual debate on platelet processing/storage strategies
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