正常骨髓基质细胞对K562细胞凋亡敏感性的影响

目的观察正常人骨髓基质细胞对白血病敏感细胞株K562细胞凋亡易感性的影响,并研究其作用机制。方法建立正常人骨髓基质细胞的体外培养体系及其与K562细胞共培养的体系;流式细胞仪检测Annexin V阳性的早期凋亡细胞;电镜下观察凋亡形态学改变;流式细胞仪检测bcl-2,活化的胱冬氨酸蛋白酶（caspaae）-3的表达变化。结果与单独K562细胞培养相比,与正常人骨髓基质细胞共培养的K562细胞,分别经阿糖胞苷作用后,共培养体系下其凋亡率下降,电镜下细胞凋亡的形态改变减少或消失,而且bcl-2蛋白表达上调,活化的caspase-3表达减弱。结论正常人骨髓基质细胞可促进白血病细胞株K562细胞的增殖,降低K562细胞对阿糖胞苷的凋亡易感性,其作用机制中包括影响凋亡相关蛋白bcl-2和caspase-3的表达。

Effects and mechanisms of bone marrow stromal cells on apoptotic sensitivity of leukemia cell line K562

Objective To investigate the effects and mechanisms of the normal bone marrow stromal cells (BMSCs) on chemosensitivity of K562 cell line in vitro. Methods Culture system of BMSCs and co-culture system of K562 cells and BMSCs in vitro were established. Expressions of active caspase-3 and bcl-2 were detected by flow cytometry using Annexin V FIFC staining; morphological assessment of apoptosis was performed with transmission electron microscope. Results Compared with K562 cells treated by Ara-C without BMSCs, the percentage of Annexin V-positive cells, apoptotic ratio, apoptotic morphological changes, and the expression of active caspase-3 decreased while bcl-2 increased in K562 cells treated by Ara-C co-cultured with BMSCs. Conclusion Normal bone marrow stromal cells can promote the proliferation of K562 cells, prevent Ara-C-induced apoptosis in K562 cells via modulation of bcl-2 and active caspase-3.