Proteomics

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Delaying aging and enhancing repair of the aged CNS myelin by β-NMN requires SIRT2

ABSTRACT: Myelin aging is a driving force of CNS aging, and age-dependent declined efficiency of remyelination caused by impaired differentiation capacity of aged oligodendrocyte precursor cell (OPC) is a major cause of demyelinated diseases. Revealing how differentiation capacity of aged OPC is affected metabolically holds the key to find new way to rejuvenate the aged OPC. Here we screened out that NAD+ is one of the top metabolites impaired in premature aging OPC. Supplementing β-nicotinamide mononucleotide (β-NMN), an immediate NAD+ precursor, delays CNS myelin aging, promotes differentiation of aged OPC, and therapeutically and preventively rejuvenates remyelination in the aged CNS both ultra-structurally and functionally. To explore the molecular mechanisms underlying the enhancing remyelination by NAD+ supplementation, using LC-MS we investigated the changes of proteome differentially regulated by NAD+ or DMSO in cultured OPC from P0 rat brain.

ORGANISM(S): Rattus Norvegicus

SUBMITTER: Jing-Wei Zhao  

PROVIDER: PXD022046 | iProX | Sun Oct 18 00:00:00 BST 2020

REPOSITORIES: iProX

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The age-dependent decline in remyelination potential of the central nervous system during ageing is associated with a declined differentiation capacity of oligodendrocyte progenitor cells (OPCs). The molecular players that can enhance OPC differentiation or rejuvenate OPCs are unclear. Here we show that, in mouse OPCs, nuclear entry of SIRT2 is impaired and NAD<sup>+</sup> levels are reduced during ageing. When we supplement β-nicotinamide mononucleotide (β-NMN), an NAD<sup>+</sup> precursor, nu  ...[more]

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