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目的:探讨慢性髓系白血病(CML)细胞系K562细胞衍生的微泡(microvesicles,MVs)对其自身增殖凋亡的影响及机制。方法:提取K562细胞培养上清MVs,PKH26标记后与人脐静脉内皮细胞(HUVEC)共同孵育,荧光显微镜下观察;不同浓度K562-MVs与细胞共孵育48h后,CCK8法观察细胞增殖变化,流式细胞分析术检测细胞凋亡率,半定量RT-PCR检测bcl-2基因的表达变化。结果:K562-MVs与HUVEC膜相融合;K562-MVs 60μg/ml实验组细胞增殖轻微受抑,与对照组比较差异无统计学意义(P>0.05),120、200、300、400μg/ml实验组细胞增殖增加,而且随着剂量的增加促增殖率逐渐增加,各作用组与对照组之间及各作用组间差异有统计学意义(P<0.05);K562-MVs 120μg/ml作用组与对照组相比细胞凋亡率下降(P<0.05),bcl-2基因的表达水平上调。结论:K562-MVs并非毫无意义的细胞碎片,而是具有生物活性的信息载体分子,可以通过与细胞膜相融合的方式传递细胞信号。K562-MVs可能通过上调抗凋亡基因bcl-2的表达水平,发挥其促增殖抗凋亡作用。
Objective: To investigate the effect and mechanism of microvesicles (MVs) derived from chronic myeloid leukemia (CML) cell line K562 on proliferation and apoptosis. Methods: K562 cell culture supernatants were harvested and incubated with human umbilical vein endothelial cells (HUVECs) and incubated with K562-MVs for 48h. The proliferation of K562-MVs was observed by flow cytometry Apoptosis rate was detected by the method of cell analysis. The expression of bcl-2 gene was detected by semi-quantitative RT-PCR. Results: K562-MVs fused with HUVEC membrane; K562-MVs 60μg / ml experimental group slightly inhibited cell proliferation, compared with the control group showed no significant difference (P> 0.05), 120,200,300,400μg / ml experiment (P <0.05); K562-MVs 120μg / ml group had no significant difference with the control group and the control group Compared with the control group, the apoptosis rate decreased (P <0.05), the expression of bcl-2 gene was up-regulated. CONCLUSIONS: K562-MVs are not meaningless cell fragments but rather bio-active information carrier molecules that can transmit cellular signals by fusion with the cell membrane. K562-MVs may exert its antiproliferative effects on proliferation by up-regulating the expression of anti-apoptotic gene bcl-2.