One of the most primitive of host‐defence mechanisms is haemostasis, the ability to control blood loss. In response to vascular trauma, platelets rapidly adhere to the exposed subendothelial matrix, a process that ultimately results in the sealing of the vessel by a plug of platelets stabilised by fibrin. Paradoxically, it is the same cascade of events that leads to thrombosis and vessel occlusion, resulting in heart attack and stroke. The molecular events involved in platelet adhesion have therefore been the subject of intense investigation. In all but the largest blood vessels, the initial contact adhesion of platelets is mediated by subendothelial matrix bound von Willebrand Factor (v WF) and a specific v WF receptor on platelets, the glycoprotein (GP) Ib‐ V‐IX complex. Our understanding of this process arose from analysis of two congenital bleeding disorders, von Willebrand's disease and the Bernard‐Soulier syndrome, in which v WF or the GP Ib‐ V‐IX, respectively, are either absent or dysfunctional. This overview discusses our current molecular understanding of platelet adhesion and how engagement of v WF by the GP lb‐ V‐IX complex on platelets initiates the subsequent events in platelet activation leading to either haemostasis or thrombosis.
|Number of pages||9|
|Journal||Australian and New Zealand Journal of Medicine|
|Publication status||Published - 1 Jan 1995|
- glycoprotein Ib‐V‐IX complex.
- Platelet adhesion
- von Willebrand factor