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NG2 glia are required for maintaining microglia homeostatic state


Liu, Yingjun; Aguzzi, Adriano (2019). NG2 glia are required for maintaining microglia homeostatic state. Glia:glia.23721.

Abstract

Microglia play vital roles in the health and diseases of the central nervous system. Loss of microglia homeostatic state is a key feature of brain aging and neurodegeneration. However, the mechanisms underlying the maintenance of distinct microglia cellular states are largely unclear. Here, we show that NG2 glia, also known as oligodendrocyte precursor cells, are essential for maintaining the homeostatic microglia state. We developed a highly efficient and selective NG2 glia depletion method using small‐molecule inhibitors of platelet‐derived growth factor (PDGF) signaling in cultured brain slices. We found that loss of NG2 glia abolished the homeostatic microglia signature without affecting the disease‐associated microglia profiles. Similar findings were also observed in vivo by genetically depleting NG2 glia or conditionally inhibiting NG2 glia PDGF signaling in the adult mouse brain. These data suggest that NG2 glia exert a crucial influence onto microglia cellular states that are relevant to brain aging and neurodegenerative diseases. In addition, our results provide a powerful, convenient, and selective tool for the investigation of NG2 glia function.

Abstract

Microglia play vital roles in the health and diseases of the central nervous system. Loss of microglia homeostatic state is a key feature of brain aging and neurodegeneration. However, the mechanisms underlying the maintenance of distinct microglia cellular states are largely unclear. Here, we show that NG2 glia, also known as oligodendrocyte precursor cells, are essential for maintaining the homeostatic microglia state. We developed a highly efficient and selective NG2 glia depletion method using small‐molecule inhibitors of platelet‐derived growth factor (PDGF) signaling in cultured brain slices. We found that loss of NG2 glia abolished the homeostatic microglia signature without affecting the disease‐associated microglia profiles. Similar findings were also observed in vivo by genetically depleting NG2 glia or conditionally inhibiting NG2 glia PDGF signaling in the adult mouse brain. These data suggest that NG2 glia exert a crucial influence onto microglia cellular states that are relevant to brain aging and neurodegenerative diseases. In addition, our results provide a powerful, convenient, and selective tool for the investigation of NG2 glia function.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Uncontrolled Keywords:Cellular and Molecular Neuroscience, Neurology
Language:English
Date:13 September 2019
Deposited On:20 Dec 2019 13:37
Last Modified:20 Dec 2019 13:37
Publisher:Wiley-Blackwell Publishing, Inc.
ISSN:0894-1491
OA Status:Green
Publisher DOI:https://doi.org/10.1002/glia.23721
PubMed ID:31518022
Project Information:
  • : FunderH2020
  • : Grant ID670958
  • : Project TitleFunction and malfunction of the prion protein
  • : FunderSNSF
  • : Grant ID31003A_179040
  • : Project TitleThe prion protein in health and disease
  • : FunderNomis Foundation
  • : Grant ID
  • : Project TitleEXPLORING THE LOCALES OF COGNITIVE DECLINE: CELLULAR AND MOLECULAR 3D ATLASES OF BRAIN PATHOLOGY IN AGING AND IN NEURODEGENERATION
  • : FunderSystemsX.ch
  • : Grant ID
  • : Project TitleSystems Biology of Prion Diseases
  • : FunderCRPP
  • : Grant ID
  • : Project TitleSmall RNAs

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