Mitochondrial respiration defects modulate differentiation but not proliferation of hematopoietic stem and progenitor cells.

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.

• Authors: Shin-Ichi Inoue, Shinichi Noda, Koutarou Kashima, Kazuto Nakada, Jun-Ichi Hayashi, Hiroyuki Miyoshi
• Journal: FEBS letters (FEBS Lett) Vol. 584 Issue 15 Pg. 3402-9 (Aug 04 2010) ISSN: 1873-3468 [Electronic] England
• PMID: 20600007 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright (c) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Chemical References

• DNA, Mitochondrial
• Reactive Oxygen Species
• Adenosine Triphosphate

Topics

• Adenosine Triphosphate (metabolism)
• Animals
• Apoptosis
• Bone Marrow Cells (cytology)
• Cell Cycle
• Cell Differentiation
• Cell Lineage (genetics)
• Cell Proliferation
• Cell Respiration
• DNA, Mitochondrial (metabolism)
• Gene Expression Regulation, Developmental
• Hematopoiesis
• Hematopoietic Stem Cells (cytology, metabolism)
• Mice
• Mitochondria (metabolism)
• Reactive Oxygen Species (metabolism)