骨髓间充质干细胞向胶质瘤迁移机制的实验研究  

The study on the migration mechanism of bone marrow-derived mesenchymal stem cells towards glioma

作　　者：程鹏[1] 高志强[2] 胡宜[2] 刘云会[2] 

机构地区：[1]中国医科大学附属第一医院神经外科,辽宁沈阳110001 [2]中国医科大学附属盛京医院神经外科,辽宁沈阳110004

出　　处：《中华神经外科疾病研究杂志》2013年第3期214-217,共4页Chinese Journal of Neurosurgical Disease Research

基　　金：国家自然科学基金资助项目(30901781);辽宁省博士启动基金资助项目(20091107)

摘　　要：目的探讨血管内皮生长因子(VEGF)在大鼠骨髓间充质干细胞(BMSCs)向C6胶质瘤迁移中的作用。方法直接贴壁法分离培养骨髓间充质干细胞。建立体外迁移模型检测大鼠重组VEGF164诱导BMSCs迁移的效果。利用磷酸肌醇3-激酶(PI3K)特异性抑制剂LY294002,分析PI3K在VEGF164诱导BMSCs迁移过程中的作用。检测C6细胞诱导BMSCs迁移的效果,分析VEGF在这一过程中的作用。结果通过直接贴壁法获得了纯化的BMSCs。20 ng/ml VEGF164能诱导BMSCs发生定向迁移,这一迁移过程能被LY294002所抑制。在加入VEGF中和抗体后,向C6细胞发生迁移的BMSCs数量减少。结论 VEGF164可以诱导BMSCs发生定向迁移,PI3K参与了这一过程的信号转导。VEGF是诱导BMSCs向C6胶质瘤定向迁移的细胞因子之一。Objective To explore the effect of vascular endothelial growth factor （VEGF） on the directional migration of rat bone marrow-derived mesenchymal stem cells （BMSCs） towards C6 glioroma cells. Methods BMSCs were isolated and cultured by direct adherent culture method. In vitro migration model was established. The effect of rat recombinant VEGF164 on the migration of BMSCs was investigated, and the regulatory role of phosphoinositide-3- kinase （PI3K） in this migration was analyzed by utilizing LY294002, a PI3K specific inhibitor. The chemotactic effect of C6 cells on BMSCs and the impact of VEGF on this process were studied. Results BMSCs were successive subculture and purified by direct adherent culture method. VEGF164 at the concentration of 20 ng/ml had the capacity of inducing BMSCs to migrate directionally, which could be inhibited by LY2941XI2. After adding anti-VEGF neutralizing antibody, the number of BMSCs migrating towards C6 cells was decreased. Condusion VEGF164 can induce BMSCs to migrate directionally, and PI3K signaling pathway is correlated with the signal transduction of this migration. VEGF is one of cytokines mediating the migration of BMSCs towards C6 glioma.

关 键 词：骨髓间充质干细胞 迁移 血管内皮生长因子 胶质瘤 磷酸肌醇3-激酶 

分 类 号：R739.41[医药卫生—肿瘤]