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10.1101/2021.05.01.442279

http://scihub22266oqcxt.onion/10.1101/2021.05.01.442279
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33972943!8109205!33972943
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suck abstract from ncbi


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pmid33972943      bioRxiv 2021 ; ä (ä): ä
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  • Signaling through FcgammaRIIA and the C5a-C5aR pathway mediates platelet hyperactivation in COVID-19 #MMPMID33972943
  • Apostolidis SA; Sarkar A; Giannini HM; Goel RR; Mathew D; Suzuki A; Baxter AE; Greenplate AR; Alanio C; Abdel-Hakeem M; Oldridge DA; Giles J; Wu JE; Chen Z; Huang YJ; Pattekar A; Manne S; Kuthuru O; Dougherty J; Weiderhold B; Weisman AR; Ittner CAG; Gouma S; Dunbar D; Frank I; Huang AC; Vella LA; Reilly JP; Hensley SE; Rauova L; Zhao L; Meyer NJ; Poncz M; Abrams CS; Wherry EJ
  • bioRxiv 2021[May]; ä (ä): ä PMID33972943show ga
  • Patients with COVID-19 present with a wide variety of clinical manifestations. Thromboembolic events constitute a significant cause of morbidity and mortality in patients infected with SARS-CoV-2. Severe COVID-19 has been associated with hyperinflammation and pre-existing cardiovascular disease. Platelets are important mediators and sensors of inflammation and are directly affected by cardiovascular stressors. In this report, we found that platelets from severely ill, hospitalized COVID-19 patients exhibit higher basal levels of activation measured by P-selectin surface expression, and have a poor functional reserve upon in vitro stimulation. Correlating clinical features to the ability of plasma from COVID-19 patients to stimulate control platelets identified ferritin as a pivotal clinical marker associated with platelet hyperactivation. The COVID-19 plasma-mediated effect on control platelets was highest for patients that subsequently developed inpatient thrombotic events. Proteomic analysis of plasma from COVID-19 patients identified key mediators of inflammation and cardiovascular disease that positively correlated with in vitro platelet activation. Mechanistically, blocking the signaling of the FcgammaRIIa-Syk and C5a-C5aR pathways on platelets, using antibody-mediated neutralization, IgG depletion or the Syk inhibitor fostamatinib, reversed this hyperactivity driven by COVID-19 plasma and prevented platelet aggregation in endothelial microfluidic chamber conditions, thus identifying these potentially actionable pathways as central for platelet activation and/or vascular complications in COVID-19 patients. In conclusion, we reveal a key role of platelet-mediated immunothrombosis in COVID-19 and identify distinct, clinically relevant, targetable signaling pathways that mediate this effect. These studies have implications for the role of platelet hyperactivation in complications associated with SARS-CoV-2 infection. ONE-SENTENCE SUMMARY: The FcgammaRIIA and C5a-C5aR pathways mediate platelet hyperactivation in COVID-19.
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