动脉血栓性疾病如心肌梗死等危害严重。动脉血栓形成过程复杂，其中血小板表面多个胶原受体在血栓形成过程中发挥重要功能。我们的前期研究发现，III型胶原受体GPR56高表达于人和小鼠血小板表面；利用GPR56敲除小鼠，证实GPR56缺失能够显著抑制III型胶原引起的血小板聚集，以及血小板在III型胶原上的铺展；进一步研究结果显示，GPR56缺失明显延缓颈动脉血栓形成。这些研究结果首次揭示了黏附GPCR受体GPR56在血小板活化和动脉血栓形成过程中的重要功能。围绕这些前期发现，本课题将结合多种生物学技术和小鼠模型，探究患者血小板GPR56表达水平及功能与心肌梗死的相关性；阐明GPR56介导血小板活化和动脉血栓形成的作用模式，以及GPR56介导的关键分子通路；探讨GPR56胞外氨基末端多肽抗血小板活化和动脉血栓形成的可能性，为研发以GPR56为靶的抗栓药物提供重要理论基础。

Arterial thrombosis such as myocardial infarction is a severe disease. The process of arterial thrombosis formation is complicated, and the collagen receptors on the surface of platelets play important roles in these processes. Our preliminary study demonstrated that type III collagen receptor GPR56 highly expressed in human and mouse platelet surface. Using GPR56 knockout mice, we found that GPR56 deficiency was able to significantly inhibit type III collagen induced platelet aggregation and the platelet spreading on type III collagen. Further study showed that GPR56 deficiency significantly blocked carotid artery thrombus formation. These results indicated that GPR56 plays important roles in platelet activation and arterial thrombus formation. In this application, we will further explore the correlation between myocardial infarction and the expression levels and activity of platelet GPR56, clarify the pattern of GPR56 mediated platelet activation and arterial thrombosis, elucidate the possible signaling pathways mediated by GPR56 in platelet; and investigate the effects of the peptide derived from GPR56 extracellular N terminal on platelet activation and arterial thrombosis. Eventually, the results derived from this project will supply an important theory for development of a new antithrombotic drug targeted on GPR56.