血管内皮生长因子对人慢性髓性白血病细胞系K562细胞的抗凋亡作用

Anti-apoptosis Effect of VEGF on the Human Chronic Myelocytic Leukemia Cell Line K562

为了探讨血管内皮生长因子(VEGF)对人白血病细胞增殖的影响,用形态学、DNA断裂琼脂糖凝胶电泳、流式细胞仪(FCM)DNA倍体分析观察VEGF对As2O3诱导的K562细胞凋亡的影响;采用蛋白印迹法检测不同浓度的VEGF对K562细胞bclXL、Bax和caspase3蛋白表达的影响;用RTPCR方法检测上述条件下bclXL、Bax的mRNA变化。结果表明:VEGF能阻止K562细胞发生凋亡,与细胞周期分布改变无相关性(P>0.05);随着VEGF浓度的增加K562细胞bclXL的mRNA与蛋白表达上调,Bax的蛋白表达降低;激活procaspase3→caspase3被阻止或减少。结论:通过影响bclXL/Bax表达比率可能是VEGF抑制K562细胞凋亡的机制之一。

To explore the effects of vascular endothelial growth factor （VEGF） on the mechanisms of CML pathogenesis, the effect of VEGF on K562 cell apoptosis induced by As2O3 was analyzed through morphologic observation, DNA fragmentation agarose gel electrophoresis and DNA ploidy flow cytometry analysis, and the effect of VEGF on the expression of bcl-XL, Bax and caspase-3 in K562 cells was determined by Western blot, meanwhile the expression difference between bcl-XL and Bax mRNA in above conditions was detected by RT-PCR. The results showed that after VEGF added, the apoptosis of K562 cells reduced, however, there was no significant changes in cell cycle distribution （ P 〉 0.05 ）. At the same time, following the increasing of the concentration of VEGF, expression of mRNA and protein of bcl-XL was up-regulated and the expression of Bax protein was down-regulated in K562 cells, and the activation of pro-caspase-3 into caspase-3 was inhibited or reduced, It is concluded that VEGF may suppress the apoptosis of K562 cells through its influence on the bcl-XL/Bax expression ratio in K562 cells.