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Updated: Oct 6, 2025

Generation of Oligodendrocytes and Oligodendrocyte-Conditioned Medium for Co-Culture Experiments
Published on: February 9, 2020
Lyso-Lipid-Induced Oligodendrocyte Maturation Underlies Restoration of Optic Nerve Function
Anddre Osmar Valdivia1,2, Sanjoy K Bhattacharya3,2
1Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami, Miami, Florida 33136.
Abstract:
Protein hyperdeimination and deficiency of lyso-phospholipids (LPC 18:1) has been associated with the pathology of demyelinating disease in both humans and mice. We uncovered interesting biology of LPC 18:1, in which LPC 18:1 induced optic nerve function restoration through oligodendrocyte maturation and remyelination in mouse model systems. Our in vitro studies show LPC 18:1 protection against neuron-ectopic hyperdeimination and stimulation of oligodendrocyte maturation, while in vivo investigations recorded optic nerve function improvement following optic nerve injections of LPC 18:1, in contrast with LPC 18:0. Thus, just a change in a single bond renders a dramatic alternation in biological function. The incorporation of isobaric C13-histidine in newly synthesized myelin proteins and quantitative proteome shifts are consistent with remyelination underlying restoration in optic nerve function. These results suggest that exogenous LPC 18:1 may provide a therapeutic avenue for stemming vision loss in demyelinating diseases.
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