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.

中文翻译：

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血小板因子4抑制ADAMTS13活性并调节von Willebrand因子的多聚体分布

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，后者受蛋白酶ADAMTS13控制。但是，尚不清楚什么调节ADAMTS13的活性。在这项研究中，我们调查了PF4是否可以与VWF结合并抑制ADAMTS13活性。我们发现PF4结合VWF并防止ADAMTS13活性。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。我们的数据提供了第一个证据，即PF4在原发性止血和血栓形成过程中可能在调节VWF多聚体中具有新作用。