磷脂酰肌醇3激酶通过mDial参与调控凝血酶诱导的血小板聚集  

PI3-kinase mediates thrombin-induced platelet aggregation through mDial pathway

作　　者：高广勋[1] 董娟顾[1] 顾宏涛[1] 高瑛[1] 潘耀柱[1] 王一苇[1] 杨阳[1] 陈协群[1] 

机构地区：[1]第四军医大学西京医院血液科,西安710032

出　　处：《中华血液学杂志》2010年第3期176-180,共5页Chinese Journal of Hematology

基　　金：国家自然科学基金（30670909、30900639）

摘　　要：目的探讨raDial（mammalian diaphanous1）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（P13K）对该过程的调控作用。方法采用血小板聚集仪检测P13K抑制剂和抗mDial抗体导人后对人血小板聚集率的影响；Westernblot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raDial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抗体导人血小板后能够抑制凝血酶诱导的血小板聚集；P13K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P13K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。Objective To investigate the expression of raDial （ mammalian diaphanous 1 ） in platelet and the role of raDial 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 raDial expression level between quiescent and activated platelets, mDial moved from a Triton-X100-soluble cytosolic fraction to insolub]e cytoskeleton 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 raDial transloeation. Conclusion PI3-kinase mediates the thrombin-induced platelet aggregation through radial pathway.

关 键 词：哺乳类 diaphanous 磷脂酰肌醇3激酶 血小板 凝血酶 

分 类 号：R55[医药卫生—血液循环系统疾病]