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Embryonic Stem Cells/Induced Pluripotent Stem Cells
Article first published online: 21 MAR 2011
Copyright © 2010 AlphaMed Press
Volume 29, Issue 3, pages 486–495, March 2011
How to Cite
Mandal, S., Lindgren, A. G., Srivastava, A. S., Clark, A. T. and Banerjee, U. (2011), Mitochondrial Function Controls Proliferation and Early Differentiation Potential of Embryonic Stem Cells. STEM CELLS, 29: 486–495. doi: 10.1002/stem.590
Disclosure of potential conflicts of interest is found at the end of this article.
Author contributions: S.M.: conception and design, collection and/or assembly of data, data analysis and interpretation, manuscript writing; A.G.L.: collection and/or assembly of data, data analysis and interpretation; A.S.S.: collection and/or assembly of data, manuscript writing; A.T.C.: conception and design, data analysis and interpretation, manuscript writing, final approval of manuscript, research supervision; U.B.: conception and design, data analysis and interpretation, manuscript writing, final approval of manuscript, financial support, administrative support, research supervision. A.T.C. and U.B. are the cocommunicating authors of this article.
First published online in STEM CELLSEXPRESS December 29, 2010.
- Issue published online: 21 MAR 2011
- Article first published online: 21 MAR 2011
- Accepted manuscript online: 29 DEC 2010 11:50AM EST
- Manuscript Accepted: 13 DEC 2010
- Manuscript Received: 28 JUL 2010
- Embryonic stem cells;
Pluripotent stem cells hold significant promise in regenerative medicine due to their unlimited capacity for self-renewal and potential to differentiate into any cell type of the body. In this study, we demonstrate that proper mitochondrial function is essential for proliferation of undifferentiated ESCs. Attenuating mitochondrial function under self-renewing conditions makes these cells more glycolytic-dependent, and it is associated with an increase in the mRNA reserves of Nanog, Oct4, and Sox2. In contrast, attenuating mitochondrial function during the first 7 days of differentiation results in normal repression of Oct4, Nanog, and Sox2. However, differentiation potential is compromised as revealed by abnormal transcription of multiple Hox genes. Furthermore, under differentiating conditions in which mitochondrial function is attenuated, tumorigenic cells continue to persist. Our results, therefore establish the importance of normal mitochondrial function in ESC proliferation, regulating differentiation, and preventing the emergence of tumorigenic cells during the process of differentiation. STEM CELLS 2011;486–495