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Mitochondrial dysfunction increases fatty acid β-oxidation and translates into impaired neuroblast maturation.
- Source :
-
FEBS letters [FEBS Lett] 2019 Nov; Vol. 593 (22), pp. 3173-3189. Date of Electronic Publication: 2019 Aug 31. - Publication Year :
- 2019
-
Abstract
- The metabolic transition from anaerobic glycolysis and fatty acid β-oxidation to glycolysis coupled to oxidative phosphorylation is a key process for the transition of quiescent neural stem cells to proliferative neural progenitor cells. However, a full characterization of the metabolic shift and the involvement of mitochondria during the last step of neurogenesis, from neuroblasts to neuron maturation, is still elusive. Here, we describe a model of neuroblasts, Neuro2a cells, with impaired differentiation capacity due to mitochondrial dysfunction. Using a detailed biochemical characterization consisting of steady-state metabolomics and metabolic flux analysis, we find increased fatty acid β-oxidation as a peculiar feature of neuroblasts with altered mitochondria. The consequent metabolic switch favors neuroblast proliferation at the expense of neuron maturation.<br /> (© 2019 Federation of European Biochemical Societies.)
Details
- Language :
- English
- ISSN :
- 1873-3468
- Volume :
- 593
- Issue :
- 22
- Database :
- MEDLINE
- Journal :
- FEBS letters
- Publication Type :
- Academic Journal
- Accession number :
- 31432511
- Full Text :
- https://doi.org/10.1002/1873-3468.13584