Lyso-Lipid-Induced Oligodendrocyte Maturation Underlies Restoration of Optic Nerve Function
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. Ourin vitrostudies show LPC 18:1 protection against neuron-ectopic hyperdeimination and stimulation of oligodendrocyte maturation, whilein vivoinvestigations 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.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Jan 01, 2022
- Source ID
- 10.1523/eneuro.0429-21.2022
Entities
People
- Anddre Valdivia
- Sanjoy K Bhattacharya
Organizations
- National Eye Institute
- United States Department of Defense