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[CD(34)(+)干/祖细胞与纤连蛋白黏附在慢性粒细胞白血病发病机制中的意义]

[The significance of the adhesion of CD(34)(+) stem/progenitor cells to fibronectin in the pathogenesis of chronic myelogenous leukemia].

作者信息

Li Z, Li J, Fu J, Chen S

机构信息

Institute of Hematology, People's Hospital, Beijing Medical University, Beijing 100034, China.

出版信息

Zhonghua Xue Ye Xue Za Zhi. 2000 Mar;21(3):138-40.

Abstract

OBJECTIVE

To investigate the significance of the adhesion of CD(34)(+) stem/progenitor cells to fibronectin in the pathogenesis of chronic myelogenous leukemia (CML).

METHODS

(1) Integrin beta(1) chain (CD(29)) and alpha(4) chain (CD(49d)) expressions on CD(34)(+) cells were measured by flow cytometry in 30 untreated CML patients in chronic phase (CML-CP) and 10 healthy donors. (2) The adhesion function of immunomagnetic beads selected CD(34)(+) cells to fibronectin was detected by crystal violet staining in 5 untreated CML-CP patients and 5 healthy donors. (3) The effect of fibronectin on CFU-GM colony formation of bone marrow cells in 3 CML patients and 3 healthy donors was observed by limited dilution liquid microculture.

RESULTS

(1) There was no significant difference in CD(29) and CD(49d) expressions on CD(34)(+) bone marrow cells between CML patients and healthy donors. (2) The adhesion of CD(34)(+) bone marrow cells to fibronectin decreased significantly in CML patients as compared with that in healthy donors (P < 0.01). (3) The CFU-GM colony formation was significantly inhibited by fibronectin in healthy donors (P < 0.01), but not in CML patients.

CONCLUSION

The adhesion function abnormality of CML CD(34)(+) bone marrow cells to fibronectin may underlie the abnormal proliferation of CML progenitors.

摘要

目的

探讨CD(34)(+)干/祖细胞与纤连蛋白的黏附在慢性髓性白血病(CML)发病机制中的意义。

方法

(1)采用流式细胞术检测30例未经治疗的慢性期慢性髓性白血病(CML-CP)患者及10名健康供者CD(34)(+)细胞上整合素β(1)链(CD(29))和α(4)链(CD(49d))的表达。(2)采用结晶紫染色法检测5例未经治疗的CML-CP患者及5名健康供者经免疫磁珠分选的CD(34)(+)细胞对纤连蛋白的黏附功能。(3)采用有限稀释液体微量培养法观察3例CML患者及3名健康供者骨髓细胞中纤连蛋白对CFU-GM集落形成的影响。

结果

(1)CML患者与健康供者CD(34)(+)骨髓细胞上CD(29)和CD(49d)的表达无显著差异。(2)与健康供者相比,CML患者CD(34)(+)骨髓细胞对纤连蛋白的黏附显著降低(P < 0.01)。(3)纤连蛋白显著抑制健康供者的CFU-GM集落形成(P < 0.01),但对CML患者无此作用。

结论

CML患者CD(34)(+)骨髓细胞对纤连蛋白的黏附功能异常可能是CML祖细胞异常增殖的基础。

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