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10.1186/s13075-017-1458-y

http://scihub22266oqcxt.onion/10.1186/s13075-017-1458-y
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suck abstract from ncbi


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pmid29141676      Arthritis+Res+Ther 2017 ; 19 (ä): ä
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  • Platelets are activated in ANCA-associated vasculitis via thrombin-PARs pathway and can activate the alternative complement pathway #MMPMID29141676
  • Miao D; Li DY; Chen M; Zhao MH
  • Arthritis Res Ther 2017[]; 19 (ä): ä PMID29141676show ga
  • Background: In this study, we investigated the mechanism of platelet activation in patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), as well as the activation of the alternative complement pathway by platelets in AAV. Methods: CD62P and platelet-leukocyte aggregates in AAV patients were tested by flow cytometry. Platelets were stimulated by plasma from active AAV patients. The effect of the thrombin-protease-activated receptors (PARs) pathway was evaluated by blocking thrombin or PAR1 antagonists. After platelets were activated by plasma from AAV patients, Ca/Mg-Tyrode?s buffer and Mg-EGTA buffer were used to measure complement activation in liquid phase and on the surface of platelets. Results: The levels of CD62P-expressing platelets and platelet-leukocyte aggregates were significantly higher in active AAV patients than those in remission and normal controls. Platelets were activated by plasma from active AAV patients (percentage of CD62P-expressing platelets, 97.7?±?3% vs. 1?±?0.2%, p?
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