K562细胞衍生的微泡对其自身作用的初步探索  

The initial exploration of effect of K562-derived microvesicles on their parental cells

作　　者：李娟娟[1] 郭冬梅[1] 陈小梅[1] 杨琰[1] 张兰男[1] 黄士昂[1] 李欣[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院干细胞中心,武汉430022

出　　处：《临床血液学杂志》2012年第2期178-181,共4页Journal of Clinical Hematology

摘　　要：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 of microvesicles（MVs）derived from K562 cells on the proliferation and apoptosis of their parental cell and analyze relevant mechanism.Method：K562-MVs were extracted from cell culture supernanant and labeled with a PKH26 red fluorescent labeling kit.Human umbilical vein endothelial cells（HUVEC）were incubated with the PKH26-labeled K562-MVs for 10 h and subjected to fluorescence microscope and photographed.K562 cells were incubated with different concentrations of K562-MVs for 48 h.Cell proliferation was assayed with CCK8 kit and cell apoptosis was analyzed with Flow cytometry.Expression of bcl-2 was examined by semi-quantitative RT-PCR.Result：K562-MVs could integrated with HUVEC cells.And K562-MVs could promote proliferation of K562 cell with the concentration of more than 60 μg/ml.The proliferation rate was concentration-dependent,and besides,differences of proliferation rates between each group were statistically significant.Compare to the control group,apoptosis rate decreased and expression level of bcl-2 increased in the 120 μg/ml group（P0.05）.Conclusion：K562-MVs are not meaningless cell debris,but the information carrier with bioactive molecules.K562-MVs can promote their parental cells proliferation and inhibit their apoptosis.K562-MVs may play its anti-apoptotic effect via increasing expression level of bcl-2.

关 键 词：白血病 髓系 慢性 K562 微泡 细胞增殖 细胞凋亡 BCL-2 

分 类 号：R733.72[医药卫生—肿瘤]