Bioactive lipid mediator class switching regulates myogenic cell progression and muscle regeneration

Paul Fabre, Thomas Molina, Jessica Larose, Karine Greffard, Gregory Généreux-Gamache, Alyson Deprez, Inès Mokhtari, Ornella Pellerito, Elise Duchesne, Junio Dort, Jean-François Bilodeau and Nicolas A. Dumont ()
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Paul Fabre: CHU Sainte-Justine Research Center
Thomas Molina: CHU Sainte-Justine Research Center
Jessica Larose: CHU de Québec-Laval University Research Center
Karine Greffard: CHU de Québec-Laval University Research Center
Gregory Généreux-Gamache: CHU Sainte-Justine Research Center
Alyson Deprez: CHU Sainte-Justine Research Center
Inès Mokhtari: CHU Sainte-Justine Research Center
Ornella Pellerito: CHU Sainte-Justine Research Center
Elise Duchesne: Université Laval
Junio Dort: University of Ottawa
Jean-François Bilodeau: CHU de Québec-Laval University Research Center
Nicolas A. Dumont: CHU Sainte-Justine Research Center

Nature Communications, 2025, vol. 16, issue 1, 1-16

Abstract: Abstract The muscle stem cell niche is well-described as influencing myogenic cell fate decision; however, the intrinsic mechanisms driving muscle stem cell progression during myogenesis are not yet fully elucidated. Here, we demonstrate that bioactive lipid class switching, an auto-regulatory mechanism originally described during the inflammatory process, is conserved during myogenesis. During the transition from proliferation to differentiation, myogenic cells shift from pro-inflammatory to pro-resolution pathways, a process partially mediated by 15Δ-PGJ2 that promotes the expression of the prostaglandin inactivation enzyme 15-hydroxyprostaglandin dehydrogenase. Using pharmacological inhibitors and knockout models of the pro-resolution enzyme 15-lipoxygenase, we show that blocking the bioactive lipid class switching impairs myoblast differentiation in vitro and muscle regeneration in vivo. Administration of the pro-resolving mediator Protectin-D1 restores myogenesis, enhances muscle regeneration post-injury and improves muscle phenotype in a dystrophic mouse model. Overall, these findings provide a better comprehension of the mechanisms regulating myogenic progression, which opens new therapeutic avenues for muscle regeneration and dystrophies.

Date: 2025
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-60586-8

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DOI: 10.1038/s41467-025-60586-8

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