PT  - JOURNAL ARTICLE
AU  - Valdivia, Anddre Osmar
AU  - Bhattacharya, Sanjoy K.
TI  - Lyso-Lipid-Induced Oligodendrocyte Maturation Underlies Restoration of Optic Nerve Function
AID  - 10.1523/ENEURO.0429-21.2022
DP  - 2022 Jan 01
TA  - eneuro
PG  - ENEURO.0429-21.2022
VI  - 9
IP  - 1
4099  - http://www.eneuro.org/content/9/1/ENEURO.0429-21.2022.short
4100  - http://www.eneuro.org/content/9/1/ENEURO.0429-21.2022.full
SO  - eNeuro2022 Jan 01; 9
AB  - 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.