端粒长度、MRE11和Ku80在再生障碍性贫血中的表达及其与发病相关性研究

Telomere Length,Expression of MRE11 and Ku80 in Patients with Aplastic Anemia and Their Correlation with Pathogenesis

目的:检测再生障碍性贫血(aplastic anemia,AA)患者骨髓单个核细胞的端粒长度、端粒相关蛋白MRE11和Ku80基因表达水平,探讨它们与AA发病的关系。方法:采用实时荧光定量聚合酶链反应(RT-qPCR)检测40例AA患者和20例正常对照者骨髓单个核细胞中端粒长度、MRE11和Ku80 mRNA表达情况,并进行相关性比较。结果:AA患者端粒长度、MRE11 mRNA和Ku80 mRNA表达水平均较正常对照组明显降低(P<0.05);年龄≥45岁的AA患者及正常对照组分别较年龄<45岁的端粒长度明显缩短(P<0.05);年龄<45岁及年龄≥45岁的AA患者分别与同年龄段的对照组相比,端粒长度均明显缩短(P<0.05);端粒长度与MRE11 mRNA表达水平(r=0.054,P>0.05)和Ku80 mRNA表达水平之间无相关性(r=0.235,P>0.05)。MRE11 mRNA表达水平与Ku80mRNA表达水平之间呈正相关(r=0.863,P<0.05)。结论:端粒长度的改变在AA的发病及疾病进展中可能发挥着重要作用,MRE11和Ku80表达的降低可能参与了AA的发病过程。

Objective： To detect the expression levels of MREll and Ku^O mRNA, and telomere length in bone marrow mononuclear cells of aplastic anemia（AA） patients, and to explore their correlation with pathogenesis of aplastic anemia. Methods： Bone marrow mononuclear cells were collected from 40 cases of AA and 20 normal controls for detecting mRNA expression of MRE11 and Ku80 and telomere length by using real-time quantitative polymerase chain reaction （qPCR）, then MRE11, Ku80 and telomere length were analyzed for their correlation. Results ： As compared with controls, the expression levels of MRE11 and Ku80 in patients with AA were significantly reduced, and the telomere length in patients with AA was obviously shortened, respectively （ P 〈 0. 05 ）. The telomere length was significantly shorter in the persons aged ≥45 years in comparison with the AA patients and normal control younger than 45 years old （ P 〈 0. 05 ）. For the AA patients older than or equal to 45 years and less than 45 years in comparison with the controls at the same age, the telomere length was significantly shorter（ P 〈 0. 05 ）. The expression levels of MRE11 and Ku80 didn＇ t correlate with telomere length （P 〉 0. 05 ）. The mRNA expression level of MRE11 correlated positively and significantly with that of Ku80 （ r = 0. 863, P 〈 0. 05 ）. Conclusion ： The change of telomere length may play an important role in the pathogenesis and progression of aplastic anemia. The lower expression of MRE11 and Ku80 may be involved in the pathogenesis of aplastic anemia.