正常骨髓基质细胞对全反式维甲酸诱导分化HL-60细胞的作用

目的研究BMSC对ATRA抑制HL-60细胞增殖、诱导其分化的作用。方法分别将融合的基质细胞层(SC)、2%戊二醛固定的基质细胞层(FSC)和基质细胞,条件培养液(SCM)与HL-60细胞共同培养。SC、FSC、SCM组分别加或不加ATRA为实验组,另设阴性对照和ATRA对照组。通过细胞计数观察细胞增殖情况及通过细胞形态观察,NBT还原试验,分析细胞分化状态。结果细胞计数示SC、FSC、SCM各组均能抑制悬浮生长的HL-60细胞的增殖;SC和FSC能增强ATRA对HL-60细胞的抑制增殖作用(P<0·01)。SC、FSC、SCM各组的诱导分化率、NBT还原率等分化指标均与阴性对照组无差异(P>0·05);SC和FSC可促进ATRA对HL-60细胞的诱导分化作用(P<0·01)。结论BMSC可增强ATRA对悬浮生长的HL-60细胞的抑制增殖和诱导分化作用,这可能是通过BMSC与HL-60细胞之间的相互作用调节的。

Effect of normal bone marrow stromal cells (BMSC) on the inhibition of proliferation and the differentiation of the leukemia cell line HL-60 induced by the all-trans retinoic acid (ATRA)

Objective To investigate the regulation of the normal bone marrow stromal cells (BMSC) on the inhibition of proliferation and the differentiation of the leukemic cell line HL-60 induced by the all-trans retinoic acid (ATRA) when HL-60 cells were cocultured with BMSC and ATRA. Methods HL-60 cells were cocultured with confluent stromal cells (SC) or fixed confluent stromal cells (FSC) with 2% glutaraldehyde or stromal cell conditioned medium (SCM) collected from confluent cultures of stromal cells respectively. Test groups included HL-60 cells cocultured with SC or FSC or SCM in the presence or absence of ATRA. HL-60 cells in culture medium or in ATRA plates were used as control groups. The proli-feration of HL-60 cells was studied by cell counting and the differentiation of them was investigated by morphology and NBT reduction test. Results Cell counting indicated that the proliferations of supernatant HL-60 cells were inhibited in SC, FSC and SCM groups; SC and FSC enhanced the inhibition of the proliferation of HL-60 cells cocultured with ATRA (P<0.01); Of SC, FSC and SCM groups the differentiation and NBT reduction test showed no differences compared with medium control group (P>0.05). SC and FSC improved the differentiation of HL-60 cells by ATRA (P<0.01). Conclusion BMSC enhances the inhibition of proliferation and induces the differentiation of supernatant HL-60 cells treated by ATRA. Direct cell-to-cell interaction between BMSC and HL-60 cells may be involved in this regulation.