SDF-1/CXCR4 axis in myelodysplastic syndromes: Correlation with angiogenesis and apoptosis

被引:18
|
作者
Zhang, Yizhuo [1 ]
Zhao, Haifeng [1 ]
Zhao, Dandan [2 ]
Sun, Lu [3 ]
Zhi, Yaqin [1 ]
Wu, Xiaoxiong [2 ]
Huang, Wenrong [4 ]
Da, Wanming [4 ]
机构
[1] TianJin Med Univ Canc Inst & Hosp, Dept Hematol, Key Lab Canc Prevent & Therapy, Tianjin 300060, Peoples R China
[2] First Affiliated Hosp Chinese Peoples Liberat Arm, Dept Hematol, Beijing, Peoples R China
[3] Gen Hosp Peoples Liberat Army, Dept Pathol, Beijing, Peoples R China
[4] Gen Hosp Peoples Liberat Army, Dept Hematol, Beijing, Peoples R China
基金
中国国家自然科学基金;
关键词
SDF-1/CXCR4; Angiogenesis; Apoptosis; MDS; LYMPHOBLASTIC-LEUKEMIA CELLS; BONE-MARROW; BCL-2-RELATED PROTEINS; IN-VITRO; CXCR4; EXPRESSION; CLASSIFICATION; VEGF; MDS; PROLIFERATION;
D O I
10.1016/j.leukres.2011.06.017
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
To study the role of SDF-1/CXCR4 axis in MDS, the expression of SDF-1 and CXCR4, VEGF, MVD and apoptosis were measured in MDS. The results showed that the expression of SDF-1 of the low-grade MDS is higher than that of the high-grade MDS and the control. The high-grade MDS had a significantly higher CXCR4 expression on CD34+ cell than low-grade MDS and the control. It was suggested that the SDF-1/CXCR4 axis play an important role in MDS. Apoptosis was significantly increased in low-grade MDS, compared with high-grade MDS. The expression of VEGF and MVD were higher in the high-grade MDS than in the low-grade MDS. There are positive correlations between SDF-1 and apoptosis in the low-grade MDS. For the high-grade MDS, there were positive correlations between CXCR4 and VEGF, and between SDF-1 concentration and MVD. The apoptosis is one of the hallmarks for low-grade MDS and the angiogenesis for high-grade MDS. A refined understanding of the roles that SDF-1/CXCR4 axis and its correlation with angiogenesis and apoptosis play in MDS will fuel the development of therapies that can be targeted to the SDF-1/CXCR4 axis. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:281 / 286
页数:6
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