Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/39129
Title: The ApoA-I mimetic peptide 5A enhances remyelination by promoting clearance and degradation of myelin debris
Authors: VANHERLE, Sam 
JORISSEN, Winde 
DIERCKX, Tess 
LOIX, Melanie 
GRAJCHEN, Elien 
MINGNEAU, Fleur 
GUNS, Jeroen 
GERVOIS, Pascal 
LAMBRICHTS, Ivo 
Dehairs, Jonas
Swinnen, Johannes, V
Mulder, Monique T.
Remaley, Alan T.
HAIDAR, Mansour 
HENDRIKS, Jerome 
BOGIE, Jeroen 
Issue Date: 2022
Publisher: CELL PRESS
Source: Cell Reports, 41 (6) (Art N° 111591)
Abstract: 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 indi-cate that 5A promotes remyelination by stimulating clearance and degradation of myelin debris.
Notes: Bogie, JJF (corresponding author), Hasselt Univ, Biomed Res Inst, Dept Immunol & Infect, B-3590 Diepenbeek, Belgium.; Bogie, JJF (corresponding author), Univ MS Ctr Hasselt, B-3900 Pelt, Belgium.
jeroen.bogie@uhasselt.be
Document URI: http://hdl.handle.net/1942/39129
ISSN: 2211-1247
e-ISSN: 2211-1247
DOI: 10.1016/j.celrep.2022.111591
ISI #: 000891242800004
Rights: 2022 The Author(s). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Category: A1
Type: Journal Contribution
Validations: ecoom 2023
Appears in Collections:Research publications

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