| First Author | Minchenberg SB | Year | 2017 |
| Journal | J Neuroimmunol | PubMed ID | 29113698 |
| Mgi Jnum | J:267801 | Mgi Id | MGI:6268984 |
| Doi | 10.1016/j.jneuroim.2017.10.015 | Citation | Minchenberg SB, et al. (2017) The control of oligodendrocyte bioenergetics by interferon-gamma (IFN-gamma) and Src homology region 2 domain-containing phosphatase-1 (SHP-1). J Neuroimmunol |
| abstractText | 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-gamma on metabolism and on oligodendrocytes, we addressed whether IFN-gamma may affect oligodendrocyte bioenergetics in ways relevant to CNS disease. Oligodendrocytes of mice treated with IFN-gamma showed significant reductions in aerobic glycolysis and mitochondrial respiration. As expected, IFN-gamma treatment led to the induction of STAT1 in oligodendrocytes indicating active signaling into these cells. To determine the direct effects of IFN-gamma on oligodendrocyte metabolism, cultured oligodendrocytes were treated with IFN-gamma in vitro, which resulted in suppression of glycolysis similar to oligodendrocytes of animals treated with IFN-gamma in vivo. Mice lacking SHP-1, a key regulator of IFN-gamma 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-gamma and SHP-1 control oligodendrocyte bioenergetics in ways that may relate to the role of this cytokine in CNS disease. |
