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We previously reported that in the absence of Prostaglandin D2 synthase (L-PGDS) peripheral nerves are hypomyelinated in development and that with aging they present aberrant myelin sheaths. We now demonstrate that L-PGDS expressed in Schwann cells is part of a coordinated program aiming at preserving myelin integrity. In vivo and in vitro lipidomic, metabolomic and transcriptomic analyses confirmed that myelin lipids composition, Schwann cells energetic metabolism and key enzymes controlling these processes are altered in the absence of L-PGDS. Moreover, Schwann cells undergo a metabolic rewiring and turn to acetate as the main energetic source. Further, they produce ketone bodies to ensure glial cell and neuronal survival. Importantly, we demonstrate that all these changes correlate with morphological myelin alterations and describe the first physiological pathway implicated in preserving PNS myelin. Collectively, we posit that myelin lipids serve as a reservoir to provide ketone bodies, which together with acetate represent the adaptive substrates Schwann cells can rely on to sustain the axo-glial unit and preserve the integrity of the PNS.
Pubmed ID: 38496560
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This polyclonal targets IgY
View all literature mentionsThis monoclonal targets beta-Tubulin
View all literature mentionsThis monoclonal targets Myelin Basic Protein (SMI 99) Purified
View all literature mentionsThis monoclonal targets Myelin Basic Protein
View all literature mentionsThis monoclonal targets Neurofilaments Phosphorylated (SMI 31)
View all literature mentionsThis unknown targets Po
View all literature mentionsThis unknown targets TurboGFP
View all literature mentionsThis polyclonal secondary targets IgY (H+L)
View all literature mentionsThis unknown targets Calnexin
View all literature mentionsThis polyclonal secondary targets IgG (H+L)
View all literature mentionsThis polyclonal targets IgG
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