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      The control of oligodendrocyte bioenergetics by interferon-gamma (IFN-γ) and Src homology region 2 domaincontaining phosphatase-1 (SHP-1)

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          Abstract

          Glycolysis and mitochondrial respiration are essential for oligodendrocyte metabolism in both the developing and adult CNS. Based on recent reports on the effects of the proinflammatory cytokine IFN-γ on metabolism and on oligodendrocytes, we addressed whether IFN-γ may affect oligodendrocyte bioenergetics in ways relevant to CNS disease. Oligodendrocytes of mice treated with IFN-γ showed significant reductions in aerobic glycolysis and mitochondrial respiration. As expected, IFN-γ treatment led to the induction of STAT1 in oligodendrocytes indicating active signaling into these cells. To determine the direct effects of IFN-γ on oligodendrocyte metabolism, cultured oligodendrocytes were treated with IFN-γ in vitro, which resulted in suppression of glycolysis similar to oligodendrocytes of animals treated with IFN-γ in vivo. Mice lacking SHP-1, a key regulator of IFN-γ and STAT1 signaling in CNS glia, had high constitutive levels of STAT1 and decreased aerobic glycolysis and mitochondrial respiration rates relative to wild type mouse oligodendrocytes. Together, these data show that IFN-γ and SHP-1 control oligodendrocyte bioenergetics in ways that may relate to the role of this cytokine in CNS disease.

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          Author and article information

          Journal
          8109498
          4636
          J Neuroimmunol
          J. Neuroimmunol.
          Journal of neuroimmunology
          0165-5728
          1872-8421
          13 November 2017
          28 October 2017
          15 June 2019
          15 June 2020
          : 331
          : 46-57
          Affiliations
          [1 ]Department of Microbiology and Immunology, SUNY Upstate Medical University, 750 East Adams Street, Syracuse, N.Y
          [2 ]Department of Neurology, SUNY Upstate Medical University, 750 East Adams Street, Syracuse, New York
          Author notes
          [* ]Corresponding author: Correspondence to Paul T. Massa, MassaP@ 123456upstate.edu
          Article
          PMC5924629 PMC5924629 5924629 nihpa918196
          10.1016/j.jneuroim.2017.10.015
          5924629
          29113698
          6b41ed61-b7f2-4a1f-87b5-9c3afb01a59e
          History
          Categories
          Article

          Mitochondria,Metabolism,SHP-1 [PTPN6],Cytokine signaling,Interferon gamma [IFN-γ],Glycolysis

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