抑癌基因PTEN是PTEN/PI3K/Akt信号通路的一员，该通路在多种生理过程中发挥作用；同时PI3K也是胶原-GPVI介导血小板活化过程中的关键因素，但PTEN在血小板中的作用鲜有报道。前期试验中，我们在国际上首次发现血小板高表达PTEN，证实PTEN是胶原引起血小板活化过程中的一个重要负性调控分子，可通过PI3K/Akt依赖和非依赖两种方式参与信号传递，但PTEN通过PI3K/AKT非依赖途径的调控机制仍未明确。本研究拟采用巨核系PTEN缺失小鼠，应用多种血小板受体和激酶拮抗剂/抑制剂，系统分析PTEN对血小板多种经典活化信号转导通路如PI3K/Akt、PLC/PKC通路等的调节作用以及其自身的受调机制；通过FeCl3诱导的血栓模型研究巨核系PTEN敲除小鼠血栓形成规律。上述研究有助于阐明PTEN调节血小板活化在血栓形成中的作用，为开发新的抗血栓药物、指导临床治疗出凝血疾病提供依据。

Tumor suppressor gene PTEN is a member of PTEN/PI3K/Akt signal pathway, which is an important pathway regulating the signaling of multiple biologic processe. PI3K plays an important role in collage-GPVI-mediated platelet activation, yet the role of PTEN in platelet activation is rarely reported. The results from our previous experiments showed that high expression of PTEN in platelets was confirmed. We also found PTEN apparently regulates collagen-induced platelet activation through PI3K/Akt-dependent and -independent signaling pathways. Further experimentation will be needed to identify the mechanism of PTEN in platelet activation. In this study PF4-Cre (megakaryocyte PTEN-/-) mice was adopted, using a variety of platelet receptors and kinases antagonist and inhibitor to analize PTEN's role in classic platelet activation of signal transduction pathways such as PI3K/Akt, PLC/PKC and so on, including its self-regulation mechanism. Thrombus model induced by FeCl3 in PTEN knockout mice are used to study the thrombsis formation mechanism. All these results are contributed to elucidate the mechanism of PTEN in platelet activation, providing new ideas for the development of new antithrombotic drugs and clinical treatment of hrombosis and hemostasis disease .