The ApoA-I mimetic peptide 5A enhances remyelination by promoting clearance and degradation of myelin debris

Sam Vanherle, Winde Jorissen, Tess Dierckx, Melanie Loix, Elien Grajchen, Fleur Mingneau, Jeroen Guns, Pascal Gervois, Ivo Lambrichts, Jonas Dehairs, Johannes V. Swinnen, Monique T. Mulder, Alan T. Remaley, Mansour Haidar, Jerome J.A. Hendriks, Jeroen J.F. Bogie*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

4 Citations (Scopus)
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The progressive nature of demyelinating diseases lies in the inability of the central nervous system (CNS) to induce proper remyelination. Recently, we and others demonstrated that a dysregulated innate immune response partially underlies failure of CNS remyelination. Extensive accumulation of myelin-derived lipids and an inability to process these lipids was found to induce a disease-promoting phagocyte phenotype. Hence, restoring the ability of these phagocytes to metabolize and efflux myelin-derived lipids represents a promising strategy to promote remyelination. Here, we show that ApoA-I mimetic peptide 5A, a molecule well known to promote activity of the lipid efflux transporter ABCA1, markedly enhances remyelination. Mechanistically, we find that the repair-inducing properties of 5A are attributable to increased clearance and metabolism of remyelination-inhibiting myelin debris via the fatty acid translocase protein CD36, which is transcriptionally controlled by the ABCA1-JAK2-STAT3 signaling pathway. Altogether, our findings indicate that 5A promotes remyelination by stimulating clearance and degradation of myelin debris.

Original languageEnglish
Article number111591
JournalCell Reports
Issue number6
Publication statusPublished - 8 Nov 2022

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