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目的探讨维甲酸综合征(RAS)发生的分子机制及防治方法。方法用微重力旋转培养系统进行维甲酸诱导分化的急性早幼粒细胞白血病患者白血病(APL-ATRA)细胞浸润人肺组织的体外实验,用地塞米松(Dex)、阿糖胞苷(Ara-C)和柔红霉素(DNR)对 APL-ATRA 细胞的黏附、迁移和浸润能力进行干预,用逆转录-聚合酶链反应(RT-PCR)检测人肺组织基质细胞衍生因子1α(SDF-1α)mRNA 的表达,用流式细胞术检测 APL-ATRA 细胞 CXCR4蛋白的表达。结果 APL-ATRA 细胞可明显浸润正常人肺组织,APL-ATRA 细胞表面 CXCR4表达水平(MFI 为30.6±1.8)明显高于诱导前的APL 细胞(9.8±4.2)。检测的6份人肺组织 SDF-1α mRNA 表达均阳性。与对照组比较,Dex 组可明显抑制 APL-ATRA 细胞的黏附和迁移能力[(46.0±3.0)%对(27.2±2.6)%;(48.2±3.0)%对(28.1±4.0)%];Ara-C 组和 DNR 组均可明显抑制 APL-ATRA 细胞的黏附、迁移和浸润能力[(46.0±3.0)%对(28.1±3.0)%、(30.2±3.2)%,(48.2±3.0)%对(29.0±4.0)%、(23.0±5.2)%,(43.6±5.0)%对(16.8±7.6)%、(17.1±6.0)%]。结论 APL-ATRA 细胞有浸润人肺组织的能力;CXCR4和 SDF-1α的高表达可能是 APL-ATRA 细胞引起人肺组织浸润的分子机制之一;Dex、Ara-C 和DNR 可抑制 APL-ATRA 细胞的黏附、迁移和浸润。
Objective To investigate the molecular mechanism of retinoic acid syndrome (RAS) and its prevention and treatment. Methods In vitro experiments of APL-ATRA cells infiltrating human lung tissue with microgravity rotation system were carried out in vitro with retinoic acid-induced differentiation of acute promyelocytic leukemia cells. Dex, Ara-C ) And daunorubicin (DNR) on the adhesion, migration and invasion of APL-ATRA cells were detected by RT-PCR. The expression of SDF-1α ) mRNA expression, the expression of CXCR4 protein in APL-ATRA cells was detected by flow cytometry. Results The APL-ATRA cells infiltrated normal lung tissue. The expression of CXCR4 on the surface of APL-ATRA cells (MFI 30.6 ± 1.8) was significantly higher than that of pre-induction APL cells (9.8 ± 4.2). The positive expression of SDF-1α mRNA in 6 human lung tissues was detected. Compared with the control group, Dex group could significantly inhibit the adhesion and migration ability of APL-ATRA cells [(46.0 ± 3.0)% vs (27.2 ± 2.6)%; (48.2 ± 3.0)% vs (28.1 ± 4.0)%] The levels of adhesion, migration and invasion in APL-ATRA cells were significantly lower in group C and group DNR (46.0 ± 3.0% vs 28.1 ± 3.0%, (30.2 ± 3.2)% and (48.2 ± 3.0)%, respectively) (29.0 ± 4.0)%, (23.0 ± 5.2)%, (43.6 ± 5.0)% versus (16.8 ± 7.6)%, (17.1 ± 6.0)%]. Conclusions APL-ATRA cells have the ability of infiltrating human lung tissue. The high expression of CXCR4 and SDF-1α may be one of the molecular mechanisms of APL-ATRA cell infiltration in human lung tissue. Dex, Ara-C and DNR can inhibit APL-ATRA Cell adhesion, migration and invasion.