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10.1371/journal.pbio.1002605

http://scihub22266oqcxt.onion/10.1371/journal.pbio.1002605
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suck abstract from ncbi


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pmid28549068
      PLoS+Biol 2017 ; 15 (5 ): e1002605
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  • Oligodendroglial myelination requires astrocyte-derived lipids #MMPMID28549068
  • Camargo N ; Goudriaan A ; van Deijk AF ; Otte WM ; Brouwers JF ; Lodder H ; Gutmann DH ; Nave KA ; Dijkhuizen RM ; Mansvelder HD ; Chrast R ; Smit AB ; Verheijen MHG
  • PLoS Biol 2017[May]; 15 (5 ): e1002605 PMID28549068 show ga
  • In the vertebrate nervous system, myelination of axons for rapid impulse propagation requires the synthesis of large amounts of lipids and proteins by oligodendrocytes and Schwann cells. Myelin membranes are thought to be cell-autonomously assembled by these axon-associated glial cells. Here, we report the surprising finding that in normal brain development, a substantial fraction of the lipids incorporated into central nervous system (CNS) myelin are contributed by astrocytes. The oligodendrocyte-specific inactivation of sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP), an essential coactivator of the transcription factor SREBP and thus of lipid biosynthesis, resulted in significantly retarded CNS myelination; however, myelin appeared normal at 3 months of age. Importantly, embryonic deletion of the same gene in astrocytes, or in astrocytes and oligodendrocytes, caused a persistent hypomyelination, as did deletion from astrocytes during postnatal development. Moreover, when astroglial lipid synthesis was inhibited, oligodendrocytes began incorporating circulating lipids into myelin membranes. Indeed, a lipid-enriched diet was sufficient to rescue hypomyelination in these conditional mouse mutants. We conclude that lipid synthesis by oligodendrocytes is heavily supplemented by astrocytes in vivo and that horizontal lipid flux is a major feature of normal brain development and myelination.
  • |*Lipid Metabolism [MESH]
  • |Animals [MESH]
  • |Astrocytes/*metabolism/pathology/ultrastructure [MESH]
  • |Biomarkers/metabolism [MESH]
  • |Crosses, Genetic [MESH]
  • |Demyelinating Diseases/*metabolism/pathology/prevention & control [MESH]
  • |Diet, High-Fat [MESH]
  • |Fatty Acid Synthase, Type I/metabolism [MESH]
  • |Gene Deletion [MESH]
  • |Glial Fibrillary Acidic Protein/genetics/metabolism [MESH]
  • |Humans [MESH]
  • |Intracellular Signaling Peptides and Proteins/genetics/*metabolism [MESH]
  • |Membrane Proteins/genetics/*metabolism [MESH]
  • |Mice, Inbred C57BL [MESH]
  • |Mice, Transgenic [MESH]
  • |Microscopy, Electron, Transmission [MESH]
  • |Mutation [MESH]
  • |Myelin Sheath/*metabolism/pathology/ultrastructure [MESH]
  • |Nerve Tissue Proteins/genetics/metabolism [MESH]
  • |Oligodendroglia/*metabolism/pathology/ultrastructure [MESH]
  • |Organ Specificity [MESH]
  • |Protein Processing, Post-Translational [MESH]


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