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Mitochondrial respiration defects modulate differentiation but not proliferation of hematopoietic stem and progenitor cells
Author(s) -
Inoue Shin-Ichi,
Noda Shinichi,
Kashima Koutarou,
Nakada Kazuto,
Hayashi Jun-Ichi,
Miyoshi Hiroyuki
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.06.036
Subject(s) - progenitor cell , haematopoiesis , microbiology and biotechnology , stem cell , biology , mitochondrion , bone marrow , progenitor , immunology
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.