Interaction of von Willebrand factor with platelets and the vessel wall
Interaction of von Willebrand factor with platelets and the vessel wall
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DOI：
10.5482/hamo-14-12-0081
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Z. Ruggeri;G. Mendolicchio
中科院分区：
文献类型：
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作者：
Z. Ruggeri;G. Mendolicchio
组织创伤后，血管损伤部位血栓形成的启动需要表面暴露的血管性血友病因子（VWF）与其主要血小板受体（糖蛋白（GP）Ib-IX-V复合物）的相互作用，以确保止血。VWF作为内皮细胞外基质（ECM）的不溶性成分，可直接启动血小板粘附。循环血浆VWF通过与暴露于流动血液的结构结合来增强基质VWF活性，特别是血管深层中的I型和III型胶原蛋白沿着内皮下层中的微纤维胶原蛋白VI型。此外，需要血浆VWF来支持血小板-血小板粘附- i。e.聚集-其促进血栓生长和固结。由于这些原因，了解血浆VWF与血小板受体的相互作用是如何调节的，特别是GPIb与可溶性而不是固定化VWF结合的任何独特特征，在血管生物学中至关重要。本文简要回顾了VWF在正常止血和病理性血栓形成中的作用，并重点介绍了VWF的研究进展和有待解决的关键问题。
Summary The initiation of thrombus formation at sites of vascular injury to secure haemostasis after tissue trauma requires the interaction of surface-exposed von Willebrand factor (VWF) with its primary platelet receptor, the glycoprotein (GP) Ib-IX-V complex. As an insoluble component of the extracellular matrix (ECM) of endothelial cells, VWF can directly initiate platelet adhesion. Circulating plasma VWF en-hances matrix VWF activity by binding to structures that become exposed to flowing blood, notably collagen type I and III in deeper layers of the vessel along with microfibrillar collagen type VI in the sub endothelium. Moreover, plasma VWF is required to support platelet-to-platelet adhesion – i. e. aggregation – which promotes thrombus growth and consolidation. For these reasons, understanding how plasma VWF interaction with platelet receptors is regulated, particularly any distinctive features of GPIb binding to soluble as opposed to immobilized VWF, is of paramount importance in vascular biology. This brief review will highlight knowledge acquired and key problems that remain to be solved to elucidate fully the role of VWF in normal haemostasis and pathological thrombosis.