Specific phospholipids regulate the acquisition of Neuronal and astroglial identities in post-mitotic cells
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Springer Nature
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Hitherto, the known mechanisms underpinning cell-fate specifcation act on neural progenitors,
afecting their commitment to generate neuron or glial cells. Here, we show that particular
phospholipids supplemented in the culture media modify the commitment of post-mitotic neural cells in
vitro. Phosphatidylcholine (PtdCho)-enriched media enhances neuronal diferentiation at the expense
of astroglial and unspecifed cells. Conversely, phosphatidylethanolamine (PtdEtn) enhances astroglial
diferentiation and accelerates astrocyte maturation. The ability of phospholipids to modify the fate
of post-mitotic cells depends on its presence during a narrow time-window during cell diferentiation
and it is mediated by the selective activation of particular signaling pathways. While PtdCho-mediated
efect on neuronal diferentiation depends on cAMP-dependent kinase (PKA)/calcium responsive
element binding protein (CREB), PtdEtn stimulates astrogliogenesis through the activation of the MEK/
ERK signaling pathway. Collectively, our results provide an additional degree of plasticity in neural cell
specifcation and further support the notion that cell diferentiation is a reversible phenomenon. They
also contribute to our understanding of neuronal and glial lineage specifcation in the central nervous
system, opening up new avenues to retrieve neurogenic capacity in the brain.
Author correction: The original version of this Article contained a typographical error in the spelling of the author Marcelo Einicker-Lamas, which was incorrectly given as Marcelo Einiker-Lamas. This has now been corrected in the PDF and HTML versions of the Article, and in the accompanying Supplementary Information file.
Author correction: The original version of this Article contained a typographical error in the spelling of the author Marcelo Einicker-Lamas, which was incorrectly given as Marcelo Einiker-Lamas. This has now been corrected in the PDF and HTML versions of the Article, and in the accompanying Supplementary Information file.
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Except where otherwise noted, this item's license is described as Attribution 4.0 International (CC BY 4.0)

