Understanding how tetraspanin superfamily members modulate platelet function

血小板是血流中的小细胞，通过粘附在一起并形成止血栓，在防止组织损伤部位的过度失血中发挥重要作用。血小板在病变血管中过度聚集会导致阻塞，并引发血栓性疾病，如心脏病发作和中风，这是西方世界人类的两大杀手。在这个建议中，我们将试图了解如何四跨膜蛋白超家族成员表达的血小板表面调节的主要血小板整合素，整合素α IIb β 3和低亲和力的IgG受体，Fc γ RIIa的功能。这项工作的目的将确定这些受体在血小板凝集中的作用，无论是在基于细胞的测定和小鼠血栓形成模型。这项工作可能会导致血栓性疾病的治疗管理的新策略。

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.