Mitochondrial dysfunction increases fatty acid β-oxidation and translates into impaired neuroblast maturation
Articolo
Data di Pubblicazione:
2019
Citazione:
Mitochondrial dysfunction increases fatty acid β-oxidation and translates into impaired neuroblast maturation / M. Audano, S. Pedretti, M. Crestani, D. Caruso, E. De Fabiani, N. Mitro. - In: FEBS LETTERS. - ISSN 0014-5793. - 593:22(2019 Nov), pp. 3173-3189. [10.1002/1873-3468.13584]
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.
Tipologia IRIS:
01 - Articolo su periodico
Keywords:
energy metabolism; mitochondria; Neuro2a cells; neuron maturation
Elenco autori:
M. Audano, S. Pedretti, M. Crestani, D. Caruso, E. De Fabiani, N. Mitro
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