Understanding how tetraspanin superfamily members modulate platelet function

血小板是血液中的小细胞，通过粘在一起形成止血栓，在防止组织损伤部位失血过多方面发挥重要作用。在患病的血管中，过多的血小板聚集会导致阻塞，并引起血栓性疾病，如心脏病发作和中风，这是西方世界人类的两大杀手。在本提案中，我们将试图了解血小板表面表达的四跨蛋白超家族成员如何调节血小板主要整合素，整合素alphaIIbbeta3和低亲和力IgG受体FcgammaRIIa的功能。这项工作的目的是在基于细胞的测定和小鼠血栓模型中确定这些受体在血小板聚集中的作用。这项工作可能导致新的策略治疗管理的血栓性疾病。

Platelets are small cells in the blood stream that play an important role in preventing excessive blood loss at sites of tissue injury by sticking together and forming a haemostatic plug. Excessive platelet clumping in diseased blood vessels can lead to blockages and cause thrombotic diseases such as heart attack and stroke, two of the biggest killers of humans in the western world. In this proposal, we will seek to understand how tetraspanin superfamily members expressed on the surface of platelets modulate the function of the major platelet integrin, integrin alphaIIbbeta3 and the low-affinity IgG receptor, FcgammaRIIa. This aims of this work will define the roles of these receptors in platelet clumping both in cell-based assays and in mouse models of thrombosis. This work could lead to new strategies for therapeutic management of thrombotic disorders.