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Elevated Serum Amyloid A Levels Contribute to Increased Platelet Adhesion in COVID-19 Patients.
Siman-Tov, Ronen; Shalabi, Rulla; Shlomai, Amir; Goldberg, Elad; Essa, Wesam; Shusterman, Eden; Ablin, Jacob N; Caspi, Michal; Rosin-Arbesfeld, Rina; Sklan, Ella H.
  • Siman-Tov R; Department of Clinical Microbiology and Immunology, The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel.
  • Shalabi R; Department of Medicine F, Rabin Medical Center, Beilinson Hospital, Petah Tikva 4941492, Israel.
  • Shlomai A; The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel.
  • Goldberg E; Department of Medicine D, Rabin Medical Center, Beilinson Hospital, Petah Tikva 4941492, Israel.
  • Essa W; Department of Medicine F, Rabin Medical Center, Beilinson Hospital, Petah Tikva 4941492, Israel.
  • Shusterman E; The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel.
  • Ablin JN; Department of Medicine F, Rabin Medical Center, Beilinson Hospital, Petah Tikva 4941492, Israel.
  • Caspi M; Department of Internal Medicine H, Tel Aviv Medical Center, Tel Aviv 6423906, Israel.
  • Rosin-Arbesfeld R; The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel.
  • Sklan EH; Department of Internal Medicine H, Tel Aviv Medical Center, Tel Aviv 6423906, Israel.
Int J Mol Sci ; 23(22)2022 Nov 17.
Article in English | MEDLINE | ID: covidwho-2116210
ABSTRACT
Coronavirus disease-19 (COVID-19) patients are prone to thrombotic complications that may increase morbidity and mortality. These complications are thought to be driven by endothelial activation and tissue damage promoted by the systemic hyperinflammation associated with COVID-19. However, the exact mechanisms contributing to these complications are still unknown. To identify additional mechanisms contributing to the aberrant clotting observed in COVID-19 patients, we analyzed platelets from COVID-19 patients compared to those from controls using mass spectrometry. We identified increased serum amyloid A (SAA) levels, an acute-phase protein, on COVID-19 patients' platelets. In addition, using an in vitro adhesion assay, we showed that healthy platelets adhered more strongly to wells coated with COVID-19 patient serum than to wells coated with control serum. Furthermore, inhibitors of integrin aIIbß3 receptors, a mediator of platelet-SAA binding, reduced platelet adhesion to recombinant SAA and to wells coated with COVID-19 patient serum. Our results suggest that SAA may contribute to the increased platelet adhesion observed in serum from COVID-19 patients. Thus, reducing SAA levels by decreasing inflammation or inhibiting SAA platelet-binding activity might be a valid approach to abrogate COVID-19-associated thrombotic complications.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Thrombosis / COVID-19 Topics: Long Covid Limits: Humans Language: English Year: 2022 Document Type: Article Affiliation country: Ijms232214243

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Thrombosis / COVID-19 Topics: Long Covid Limits: Humans Language: English Year: 2022 Document Type: Article Affiliation country: Ijms232214243