再生障碍性贫血、骨髓增生异常综合征及急性髓系白血病患者骨髓基质细胞衍生因子-1及其受体CXCR4的表达水平和意义

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目的:探讨基质细胞衍生因子-1及其受体CXCR4(SDF-1/CXCR4)在再生障碍性贫血(AA)、骨髓增生异常综合征(MDS)、急性髓系白血病(AML)发病中的作用。方法:应用酶联免疫吸附试验(ELISA)检测MDS、AA、AML患者及对照组患者(缺铁性贫血3例,营养性贫血3例)骨髓上清液中SDF-1水平,应用流式细胞仪检测MDS、AA、AML患者及对照组骨髓CD34+细胞表面表达CXCR4的情况。结果:AML、AA、MDS患者和对照组骨髓上清液中SDF-1含量分别为8125.0、6429.5、10816.2和8846.5pg/mL,AA患者的SDF-1水平分别与MDS、MDS低危组有统计学差异(P=0.001,P=0.001),AML、AA、MDS患者的SDF-1水平与对照组均无统计学差异(P>0.05)。AML、AA及对照组骨髓CD34+细胞上表达CXCR4的百分率分别为(11+16)%、(70+26)%和(20+11)%,MDS为(32+31)%。MDS按IPSS评分分为低危组及高危组,CD34+细胞CXCR4表达百分率分别为(37+33)%、(15+17)%(P=0.025)。结论:骨髓造血微环境可能通过调节AA、AML及MDS患者骨髓CD34+细胞表达CXCR4水平,对疾病产生负反馈调节,从而抑制以上3种疾病的进展。 AIM: To investigate the role of stromal cell-derived factor-1 and its receptor CXCR4 (SDF-1 / CXCR4) in the pathogenesis of aplastic anemia (AA), myelodysplastic syndrome (MDS) and acute myeloid leukemia . Methods: The levels of SDF-1 in bone marrow supernatant of patients with MDS, AA, AML and control group (3 cases of iron deficiency anemia and 3 cases of nutritional anemia) were detected by enzyme linked immunosorbent assay (ELISA). Flow cytometry The expression of CXCR4 on the surface of CD34 + cells in MDS, AA and AML patients and control group was detected. Results: The levels of SDF-1 in bone marrow supernatant of patients with AML, AA, MDS and control group were 8125.0, 6429.5, 10816.2 and 8846.5 pg / mL, respectively. The SDF-1 levels in AA patients were lower than those in MDS and MDS (P = 0.001, P = 0.001). The levels of SDF-1 in AML, AA and MDS patients were not significantly different from those in control group (P> 0.05). The percentages of CXCR4 expressed on bone marrow CD34 + cells in AML, AA and control groups were (11 + 16)%, (70 + 26)% and (20 + 11)%, respectively. According to the IPSS score, MDS was divided into low-risk group and high-risk group. The percentage of CXCR4 expression in CD34 + cells was (37 + 33)% and (15 + 17)% respectively (P = 0.025). Conclusion: The myeloid hematopoietic microenvironment may regulate the expression of CXCR4 in bone marrow CD34 + cells of patients with AA, AML and MDS to negatively regulate the disease and thus inhibit the progression of the above three diseases.
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