Mitochondrial respiration defects modulate differentiation but not proliferation of hematopoietic stem and progenitor cells |
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Authors: | Shin-Ichi Inoue Shinichi Noda Koutarou Kashima Kazuto Nakada Hiroyuki Miyoshi |
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Affiliation: | a Subteam for Manipulation of Cell Fate, RIKEN BioResource Center, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan b Graduate School of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8572, Japan |
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Abstract: | 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. |
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Keywords: | HSPCs, hematopoietic stem and progenitor cells HSCs, hematopoietic stem cells MPPs, multipotent progenitors CLPs, common lymphoid progenitors CMPs, common myeloid progenitors mtDNA, mitochondrial DNA BM, bone marrow PB, peripheral blood ROS, reactive oxygen species |
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