摘要目的 探讨mDial(mammalian diaphanous 1)在人血小板中的表达和血小板聚集过程中的作用以及磷脂酰肌醇3激酶(PI3K)对该过程的调控作用.方法 采用血小板聚集仪检测PI3K抑制剂和抗mDial抗体导入后对人血小板聚集率的影响;Western blot法检测mDial在血小板静止及活化过程中的表达及其与肌动蛋白细胞骨架的关系.结果 mDial在血小板静止、凝血酶诱导的铺展或聚集血小板内表达水平没有明显差异;凝血酶诱导血小板聚集过程中,mDial从Triton-X100可溶性(胞质)部分向Triton-X100不可溶性(细胞骨架)部分转位;抗mDial抗体导入血小板后能够抑制凝血酶诱导的血小板聚集;PI3K抑制剂渥曼青霉素及Ly294002能够抑制血小板聚集,抑制mDial从Triton-X100可溶性部分向Triton-X100不可溶性部分的转位.结论 PI3K通过mDial参与调控凝血酶诱导的血小板聚集过程中肌动蛋白细胞骨架的重构.

abstractsObjective To investigate the expression of mDial(mammalian diaphanous 1)in platelet and the role of mDial or phosphatidylinositol 3-kinase(PI3K)in the process of thrombin-induced platelet aggregation.Methods The extent of platelet aggregation was measured by a platelet aggregation system and the expression of mDial and its relation with F-actin in quiescent,spreading or aggregated platelets by Western blot.Results There was no significant difference in mDial expression level between quiescent and activated platelets.mDial moved from a Triton-X100-soluble cytosolie fraction to insoluble eytoskeleton fraction after thrombin induced platelets aggregation.Anti-mDial antibody could inhibit this aggregation.PI3K inhibitor Wortmannin or Ly294002 inhibited the thrombin induced platelet aggregation and the above mentioned mDial translocation.Conclusion PI3-kinase mediates the thrombin-induced platelet aggregation through mDial pathway.