Journal
PLOS ONE
Volume 8, Issue 12, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0082095
Keywords
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Categories
Funding
- Fundacao para a Ciencia e a Tecnologia (FCT) Portugal [PTDC/EBB-EBI/101114/2008, PTDC/EBB-EBI/120634/2010, PDTC/QUI-BIQ/120652/2010]
- Compete/FEDER/National Funds
- FCT [PEst-C/SAU/LA0001/2011]
- Swedish Foundation for Strategic Research (SRL Program)
- Swedish Research Council (DBRM)
- Karolinska Institutet (SFO Thematic Center in Stem Cells and Regenerative Medicine)
- Hjarnfonden
- [SFRH/BD/37933/2007]
- Fundação para a Ciência e a Tecnologia [SFRH/BD/37933/2007, PTDC/EBB-EBI/101114/2008, PTDC/EBB-EBI/120634/2010] Funding Source: FCT
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The mitochondrion is emerging as a key organelle in stem cell biology, acting as a regulator of stem cell pluripotency and differentiation. In this study we sought to understand the effect of mitochondrial complex III inhibition during neuronal differentiation of mouse embryonic stem cells. When exposed to antimycin A, a specific complex III inhibitor, embryonic stem cells failed to differentiate into dopaminergic neurons, maintaining high Oct4 levels even when subjected to a specific differentiation protocol. Mitochondrial inhibition affected distinct populations of cells present in culture, inducing cell loss in differentiated cells, but not inducing apoptosis in mouse embryonic stem cells. A reduction in overall proliferation rate was observed, corresponding to a slight arrest in S phase. Moreover, antimycin A treatment induced a consistent increase in HIF-1 alpha protein levels. The present work demonstrates that mitochondrial metabolism is critical for neuronal differentiation and emphasizes that modulation of mitochondrial functions through pharmacological approaches can be useful in the context of controlling stem cell maintenance/ differentiation.
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