THE MOLECULAR MECHANISM OF PLATELET-ADHESION

One of the most primitive of host-defence mechanisms is haemostasis, t he ability to control blood loss. In response to vascular trauma, plat elets rapidly adhere to the exposed subendothelial matrix, a process t hat ultimately results in the sealing of the vessel by a plug of plate lets stabilised by fibrin. Paradoxically, it is the same cascade of ev ents 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 i s mediated by subendothelial matrix bound von Wiilebrand Factor (nu WF ) and a specific nu WF receptor on platelets, the glycoprotein (GP) Ib -V-IX complex. Our understanding of this process arose from analysis o f two congenital bleeding disorders, von Willebrand's disease and the Bernard-Soulier syndrome, in which nu WF or the GP Ib-V-IX, respective ly are either absent or dysfunctional. This overview discusses our cur rent molecular understanding of platelet adhesion and how engagement o f nu WF by the GP Ib-V-IX complex on platelets initiates the subsequen t events in platelet activation leading to either haemostasis or throm bosis.