2023
Very-long-chain fatty acids induce glial-derived sphingosine-1-phosphate synthesis, secretion, and neuroinflammation
Chung H, Ye Q, Park Y, Zuo Z, Mok J, Kanca O, Tattikota S, Lu S, Perrimon N, Lee H, Bellen H. Very-long-chain fatty acids induce glial-derived sphingosine-1-phosphate synthesis, secretion, and neuroinflammation. Cell Metabolism 2023, 35: 855-874.e5. PMID: 37084732, PMCID: PMC10160010, DOI: 10.1016/j.cmet.2023.03.022.Peer-Reviewed Original ResearchConceptsExperimental autoimmune encephalomyelitisMultiple sclerosisAdministration of fingolimodFunctions of S1PNF-κB activationSphingosine-1-phosphate (S1P) synthesisS1P receptor antagonistsElevated VLCFAAutoimmune encephalomyelitisFatty acidsMacrophage infiltrationReceptor antagonistImmune cellsMouse modelTreatment avenuesVLCFA levelsFly gliaLong-chain fatty acidsGliaS1P pathwayS1PNeuroinflammationFingolimodVLCFAAbundant fatty acids
2022
Neuronal activity induces glucosylceramide that is secreted via exosomes for lysosomal degradation in glia
Wang L, Lin G, Zuo Z, Li Y, Byeon S, Pandey A, Bellen H. Neuronal activity induces glucosylceramide that is secreted via exosomes for lysosomal degradation in glia. Science Advances 2022, 8: eabn3326. PMID: 35857503, PMCID: PMC9278864, DOI: 10.1126/sciadv.abn3326.Peer-Reviewed Original Research
2020
Loss- or Gain-of-Function Mutations in ACOX1 Cause Axonal Loss via Different Mechanisms
Chung H, Wangler M, Marcogliese P, Jo J, Ravenscroft T, Zuo Z, Duraine L, Sadeghzadeh S, Li-Kroeger D, Schmidt R, Pestronk A, Rosenfeld J, Burrage L, Herndon M, Chen S, Network M, Shillington A, Vawter-Lee M, Hopkin R, Rodriguez-Smith J, Henrickson M, Lee B, Moser A, Jones R, Watkins P, Yoo T, Mar S, Choi M, Bucelli R, Yamamoto S, Lee H, Prada C, Chae J, Vogel T, Bellen H. Loss- or Gain-of-Function Mutations in ACOX1 Cause Axonal Loss via Different Mechanisms. Neuron 2020, 106: 589-606.e6. PMID: 32169171, PMCID: PMC7289150, DOI: 10.1016/j.neuron.2020.02.021.Peer-Reviewed Original ResearchConceptsSchwann cellsAxonal lossMurine Schwann cellsPrimary Schwann cellsTreatment of fliesLong-chain fatty acid β-oxidation pathwayNeuronal lossGlial lossSynaptic transmissionRate-limiting enzymeDevelopmental delayACOX1Elevated levelsFatty acid β-oxidation pathwayReactive oxygen speciesDifferent mechanismsPupal deathPatientsDominant variantFunction mutationsGliaOxygen speciesTreatmentDe novoCells