[Effect of HIF-1α on Angiogenesis-Related Factors in K562 Cells].

OBJECTIVE: To explore the mechanisms of angiogenesis in chronic myeloid leukemia (CML) through detecting the levels of angiogenesis-related factors secreted from K562 cells after overexpression and interference of HIF-1α gene in K562 cells. 目的: 通过在K562细胞过表达和干扰HIF-1α后检测K562细胞分泌血管生成相关因子的水平，探讨慢性白血病血管生成的机制. 方法: 应用携带和干扰HIF-1α基因的慢病毒转染K562细胞，将转染携带和干扰HIF-1α基因的K562细胞分别纳入过表达组、干扰组，同时以空载病毒转染K562细胞纳入对照组。3组细胞在常氧状态下培养72 h后收集细胞，通过荧光显微镜观察3组转染效率，采用RT-PCR法检测HIF-1α和血管相关生成因子mRNA表达水平，ELISA法检测培养上清中血管相关细胞因子的浓度. CONCLUSION: The positive K562 cells transfected with leutivirus have been harvested by screening with puromycin. The HIF-1α mRNA positively regulates the mRNA expression of ANG-1, ANG-2, TGF-α, VEGF in K562 cells, promotes the antocrine ability of ANG-1 and TNF-α, moreover not stimulates the autocrine of TGF-α, the up-regulation of HIF-1α expression can inhibit the expression TGF-β1 in K562 cells and the autocrine of TGF-β1. 结论: 通过嘌呤霉素筛选获得慢病毒转染K562细胞阳性细胞，HIF-1α mRNA正向调控K562细胞ANG-1、ANG-2、TGF-α、VEGF mRNA的表达，促进ANG-I和TNF-α自身分泌的能力，而不刺激TGF-α的自分泌，HIF-1α上调可抑制K562细胞TGF-β1的表达并抑制TGF-β的自分泌.