Mitochondrial respiration defects modulate differentiation but not proliferation of hematopoietic stem and progenitor cells
Mitochondrial respiration defects modulate differentiation but not proliferation of hematopoietic stem and progenitor cells
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DOI：
10.1016/j.febslet.2010.06.036
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发表时间：
2010-08-04
期刊：
影响因子：
3.5
通讯作者：
Miyoshi, Hiroyuki
中科院分区：
文献类型：
--
作者：
Inoue, Shin-Ichi;Noda, Shinichi;Miyoshi, Hiroyuki
线粒体能量产生涉及各种细胞过程。在这里，我们表明，ATP含量显着增加谱系限制的祖细胞相比，造血干细胞和祖细胞（HSPCs）或更分化的细胞。使用线粒体疾病的小鼠模型的移植分析显示，线粒体呼吸缺陷导致骨髓细胞的总数和再生活性显著降低，尽管HSPC的数量增加。HSPCs和谱系限制祖细胞的增殖活性不受ATP含量减少的影响，似乎没有相关的活性氧水平和细胞凋亡的增加。我们的研究结果表明，线粒体呼吸缺陷调节HSPC的承诺/分化为谱系限制的祖细胞。(C)2010年欧洲生物化学学会联合会。由Elsevier B. V.出版，版权所有。
Mitochondrial energy production is involved in various cellular processes. Here we show that ATP content is significantly increased in lineage-restricted progenitor cells compared with hematopoietic stem and progenitor cells (HSPCs) or more differentiated cells. Transplantation analysis using a mouse model of mitochondrial disease revealed that mitochondrial respiration defects resulted in a significant decrease in the total number and repopulating activity of bone marrow cells, although the number of HSPCs increased. The proliferative activity of HSPCs and lineage-restricted progenitor cells was not impaired by reduction of ATP content and there seems to be no associated increase in reactive oxygen species levels and apoptosis. Our findings indicate that mitochondrial respiration defects modulate HSPC commitment/differentiation into lineage-restricted progenitor cells. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.