Lyso-Lipid-Induced Oligodendrocyte Maturation Underlies Restoration of Optic Nerve Function

Anddre Osmar Valdivia, Sanjoy K. Bhattacharya

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Article numberENEURO.0429-21.2022
JournaleNeuro
Volume9
Issue number1
DOIs
StatePublished - Jan 1 2022
Externally publishedYes

Keywords

  • Deimination
  • LPC 18:1
  • Myelin
  • Oligodendrocytes
  • Optic nerve
  • Remyelination

ASJC Scopus subject areas

  • Neuroscience(all)

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