血管紧张素Ⅱ对定向造血祖细胞BFU-E体外扩增的影响  被引量:1

Research on the effect of Ang Ⅱ on committed hematopoietic progenitor BFU-E cells expansion in vitro

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作  者:黎纬明[1] 彭程[1] 李爱香[1] 马艳萍[1] 邹萍[1] 

机构地区:[1]华中科技大学同济医学院附属协和医院血液科,武汉430022

出  处:《临床血液学杂志》2003年第5期230-232,共3页Journal of Clinical Hematology

摘  要:目的:研究血管紧张素Ⅱ(AngⅡ)参与造血调控的机制及其对造血干/祖细胞BFU-E定向优势分化的作用。方法:将脐血来源的CD34^+细胞在不同的细胞因子组合中悬浮培养,使它们向红系造血祖细胞优势分化,分别在不同时间对培养细胞进行3种处理:一部分细胞提取RNA,用RT-PCR方法检测AngⅡ受体mR-NA的转录;一部分添加AngⅡ和其他细胞因子继续培养3天后转移到半固体培养基中进行集落计数;其余细胞在原来的条件下继续悬浮培养。结果:新分离的CD34^+细胞表面无AngⅡ受体mRNA的表达,此时添加AngⅡ对造血祖细胞生长无明显作用;在CD34^+向红系优势分化体系中悬浮培养7天后,细胞中能检测到AngⅡ受体mRNA的表达,此时添加AngⅡ可刺激BFU-E的扩增;在培养第14天,细胞中己无AngⅡ受体表达,此时添加AngⅡ对红系祖细胞的扩增已无明显作用。结论:红系祖细胞在分化过程中有AngⅡ受体mRNA的表达,AngⅡ可刺激早期红系造血祖细胞的增生,并可提高造血细胞向红系定向优势分化的效率。Objective:To study the effect of AngII on committed hematopoietic progenitors BFU-E ex vivo expansion and it's mechanism. Method: CD34 + cells isolated from cord blood were cultured in the presence of different cytokines combination. They are committed to erythrocytic differentiation. After different period of culture, one part of cells were isolated for RT-PCR to detect the expression of AngII receptor mRNA. One part of cells were plated into semi-solid culture medium after they were cultured for another three days with Angll. 14 days later, the effect of Ang n was detected by the enumeration of BFU-E. Result: The newly isolated CD34+ cells didn't express AngII receptor mRNA, and their growth was not influenced by AngII. When CD34+ cells were cultured for 7 days in the condition of facilitating commitment to erythrocyte differentiation, the group of cells had AngII receptor mRNA expression. AngII could stimulate BFU-E proliferation. But 14 days later, the erythrocytic committed cells were negative for AngII receptor detection. Then AngII failed its influence on erythric progenitor cells proliferation. Conclusion; AngII influenced hematopoietic cells growth by the way of receptor. It can stimulate early erythric progenitors expansion.

关 键 词:血管紧张素Ⅱ 脐血 造血祖细胞 体外扩增 造血调控 

分 类 号:R972[医药卫生—药品] R322.2[医药卫生—药学]

 

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