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Platelets are very abundant in the blood, where they play a role in hemostasis, inflammation, and immunity. When activated, platelets undergo a conformational change that allows the release of numerous effector molecules as well as the production of extracellular vesicles, which are circulating submicron vesicles (10 to 1,000 nm in diameter) released into the extracellular space. Extracellular vesicles are formed by the budding of platelet and they carry some of its contents, including nucleic acids, surface proteins, and organelles. While platelets cannot cross tissue barriers, platelet-derived extracellular vesicles can enter the lymph, bone marrow, and synovial fluid. This allows the transfer of diverse contents carried by these platelet-derived vesicles to cell recipients and organs inaccessible to platelets where they can perform many functions. This review highlights the importance of these platelet-derived extracellular vesicles under different physiological and pathophysiological conditions. [ABSTRACT FROM AUTHOR]

Platelets were isolated from healthy donors (n = 10, green dots), COVID-19 patients treated with aspirin (n = 10, red dots), or not treated with aspirin (n = 10, blue squares). Given that aspirin was found without effect on platelet functions in certain proinflammatory conditions, [15][16][27] and since it is unclear what mediates platelet activation in COVID-19, the question of whether aspirin would have any effect on platelet activation in COVID-19 patients remained to be addressed. Thus, an aspirin regimen can reduce platelet aggregation induced by low concentrations of thrombin and collagen and the production of TxB SB 2 sb , but the effects of aspirin on platelet aggregation are lost with higher concentrations of agonists. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), is spreading throughout the world at an alarming rate. [Extracted from the article]

To further explore the signaling mechanism involved in the regulatory role of PKC in thrombin-induced platelet aggregation in CD patients, we assessed the phosphorylation of PKC on Tyr SP 311 sp and Thr SP 505 sp . In human platelets, pre-treatment with the specific PKC inhibitor significantly decreased platelet activation in patients with CD. The pathogenesis of inflammatory bowel diseases (IBD), representing chronic and relapsing-remitting disorders of the gastrointestinal tract, encompasses Crohn's disease (CD) and ulcerative colitis. [Extracted from the article]

[13] Although platelets from COVID-19 patients have shown hyperreactivity, [4][5][6] no scientific data have been able to demonstrate platelet dysfunction in people injected with the Oxford-AstraZeneca vaccine. [13] Therefore, this study aimed to assess platelet function by measuring the aggregation of platelets from participants who had been injected with the Oxford-AstraZeneca vaccine compared with platelets from a cohort of healthy donors. [Extracted from the article]