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Lyso-lipid induced oligodendrocytes maturation underlie restoration of optic nerve function

ABSTRACT: Protein hyper-deimination 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 hyper-deimination and stimulation of oligodendrocyte maturation, while in vivo investigations recorded optic nerve function improvement following optic nerve injections of LPC 18:1, in contrast to 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.

ORGANISM(S): Rat Rattus Norvegicus

TISSUE(S): Cultured Cells

DISEASE(S): Eye Disease

SUBMITTER: Sanjoy K. Bhattacharya

PROVIDER: ST002047 | MetabolomicsWorkbench | Thu Dec 16 00:00:00 GMT 2021

REPOSITORIES: MetabolomicsWorkbench

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