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NG2 glial cells regulate neuroimmunological responses to maintain neuronal function and survival.


ABSTRACT: NG2-expressing neural progenitor cells (i.e., NG2 glial cells) maintain their proliferative and migratory activities even in the adult mammalian central nervous system (CNS) and produce myelinating oligodendrocytes and astrocytes. Although NG2 glial cells have been observed in close proximity to neuronal cell bodies in order to receive synaptic inputs, substantive non-proliferative roles of NG2 glial cells in the adult CNS remain unclear. In the present study, we generated NG2-HSVtk transgenic rats and selectively ablated NG2 glial cells in the adult CNS. Ablation of NG2 glial cells produced defects in hippocampal neurons due to excessive neuroinflammation via activation of the interleukin-1 beta (IL-1?) pro-inflammatory pathway, resulting in hippocampal atrophy. Furthermore, we revealed that the loss of NG2 glial cell-derived hepatocyte growth factor (HGF) exacerbated these abnormalities. Our findings suggest that NG2 glial cells maintain neuronal function and survival via the control of neuroimmunological function.

SUBMITTER: Nakano M 

PROVIDER: S-EPMC5307324 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature

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NG2 glial cells regulate neuroimmunological responses to maintain neuronal function and survival.

Nakano Masayuki M   Tamura Yasuhisa Y   Yamato Masanori M   Kume Satoshi S   Eguchi Asami A   Takata Kumi K   Watanabe Yasuyoshi Y   Kataoka Yosky Y  

Scientific reports 20170214


NG2-expressing neural progenitor cells (i.e., NG2 glial cells) maintain their proliferative and migratory activities even in the adult mammalian central nervous system (CNS) and produce myelinating oligodendrocytes and astrocytes. Although NG2 glial cells have been observed in close proximity to neuronal cell bodies in order to receive synaptic inputs, substantive non-proliferative roles of NG2 glial cells in the adult CNS remain unclear. In the present study, we generated NG2-HSVtk transgenic r  ...[more]

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