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

Expressions of stromal cell derived factor-1 and its receptor CXCR4 in patients with aplastic anemia, myeloid dysplasia syndrome and acute myelocytic leukemia

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。

Objective To investigate the role of stromal cell derived factor-1 （SDF-1） and its receptor CXCR4 in the pathogenesis of aplastic anemia （AA）, myeloid dysplasia syndrome （MDS） and acute myelocytic leukemia （AML）. Methods ELISA was used to determine the SDF-1 level in bone marrow supernatant and flow cytometry was used to measure the CXCR4 expressing CD34＋cells in patients with AA, MDS, AML and controls （iron-deficiency anemia and deficiency anemia）. Results The level of SDF-1 in bone marrow supernatant from patients with AML, AA, MDS and controls were 8125.0, 6429.5, 10816.2 and 8846.5 pg/mL, respectively. Statistically significant difference in level of SDF-1 was found between patients with AA and patients with MDS and low risk MDS （P=0.001,0.001）, and no statistical significant difference was seen between patients with AML, AA, MDS and controls （P0.05）. The percentages of CXCR4 expressing CD34 ＋ cell in patients with AML, AA, MDS and controls were （11±16）%, （70±26）%, （32±31）% and （20±11）%, respectively. MDS patients were divided into low risk and high risk groups according to IPSS score, the percentages of CXCR4 expressing CD34＋ cell in low risk and high risk MDS patients were （37±33）% and （15±17）%, respectively （P= 0.025）. Conclusions Bone marrow micro-environment might play a negative feedback role to inhibit the progression of disease by regulating the level of CXCR4 expressing CD34＋cells.