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10.1111/jth.15587

http://scihub22266oqcxt.onion/10.1111/jth.15587
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34752677!8646637!34752677
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suck abstract from ncbi


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pmid34752677      J+Thromb+Haemost 2022 ; 20 (2): 387-398
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  • Antibody-mediated procoagulant platelet formation in COVID-19 is AKT dependent #MMPMID34752677
  • Pelzl L; Singh A; Funk J; Witzemann A; Marini I; Zlamal J; Weich K; Abou-Khalel W; Hammer S; Uzun G; Althaus K; Bakchoul T
  • J Thromb Haemost 2022[Feb]; 20 (2): 387-398 PMID34752677show ga
  • BACKGROUND: Thromboembolic events are frequently reported in patients infected with the SARS-CoV-2. Recently, we observed that platelets from patients with severe COVID-19 infection express procoagulant phenotype. The molecular mechanisms that induce the generation of procoagulant platelets in COVID-19 patients are not completely understood. OBJECTIVES: In this study, we investigated the role of AKT (also known as Protein Kinase B), which is the major downstream effector of PI3K (phosphoinositid-3-kinase) (PI3K/AKT) signaling pathway in platelets from patients with COVID-19. PATIENTS AND METHODS: Platelets, Sera and IgG from COVID-19 patients who were admitted to the intensive care unit (ICU) were analyzed by flow cytometry as well as western blot and adhesion assays. RESULTS: Platelets from COVID-19 patients showed significantly higher levels of phosphorylated AKT, which was correlated with CD62p expression and phosphatidylserine (PS) externalization. In addition, healthy platelets incubated with sera or IgGs from ICU COVID-19 patients induced phosphorylation of PI3K and AKT and were dependent on Fc-gamma-RIIA (FcgammaRIIA). In contrast, ICU COVID-19 sera mediated generation of procoagulant platelets was not dependent on GPIIb/IIIa. Interestingly, the inhibition of phosphorylation of both proteins AKT and PI3K prevented the generation of procoagulant platelets. CONCLUSIONS: Our study shows that pAKT/AKT signaling pathway is associated with the formation of procoagulant platelets in severe COVID-19 patients without integrin GPIIb/IIIa engagement. The inhibition of PI3K/AKT phosphorylation might represent a promising strategy to reduce the risk for thrombosis in patients with severe COVID-19.
  • |*COVID-19[MESH]
  • |*Proto-Oncogene Proteins c-akt[MESH]
  • |Blood Platelets[MESH]
  • |Humans[MESH]
  • |Phosphatidylinositol 3-Kinases[MESH]
  • |Platelet Activation[MESH]
  • |Platelet Aggregation[MESH]
  • |Platelet Glycoprotein GPIIb-IIIa Complex[MESH]


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