血小板因子 4 抑制 ADAMTS13 活性并调节血管性血友病因子的多聚体分布。
Platelet factor 4 inhibits ADAMTS13 activity and regulates the multimeric distribution of von Willebrand factor.
机构信息
Department of Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, Ontario, Canada.
McMaster Centre for Transfusion Research, Hamilton, Ontario, Canada.
出版信息
Br J Haematol. 2020 Aug;190(4):594-598. doi: 10.1111/bjh.16553. Epub 2020 Mar 4.
The efficiency of von Willebrand factor (VWF) in thrombus formation is related to its multimeric size, which is controlled by the protease ADAMTS13. However, it is not clear what regulates ADAMTS13 activity. In this study, we investigated whether PF4 could bind to VWF and inhibit ADAMTS13 activity. We found that PF4 binds to VWF and protects against ADAMTS13 activity. We also found that VWF-PF4 complexes circulate in patients with thrombotic thrombocytopenic purpura (TTP). Our data provides the first evidence that PF4 may have a novel role in regulating VWF multimers during primary haemostasis and thrombosis.
血管性血友病因子（VWF）在血栓形成中的效率与其多聚体大小有关，而多聚体大小由蛋白酶 ADAMTS13 控制。然而，目前尚不清楚是什么调节了 ADAMTS13 的活性。在这项研究中，我们研究了 PF4 是否可以与 VWF 结合并抑制 ADAMTS13 的活性。我们发现 PF4 与 VWF 结合并保护其免受 ADAMTS13 的活性影响。我们还发现 VWF-PF4 复合物在血栓性血小板减少性紫癜（TTP）患者中循环。我们的数据首次提供了证据，表明 PF4 可能在初级止血和血栓形成过程中调节 VWF 多聚体方面发挥新的作用。
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