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Sci Rep. 2018 Feb 6;8(1):2524. doi: 10.1038/s41598-018-20980-3.

Liver X Receptor exerts a protective effect against the oxidative stress in the peripheral nerve.

Author information

1
Paris Descartes University, INSERM UMR-S 1124, Faculty of Basic and Biomedical Sciences, 45 rue des Saints-Pères, 75270, Paris Cedex 6, France.
2
American University of Beirut, Department of Anatomy, Cell Biology and Physiological Sciences, PO Box 11-0236, Riad El-Solh, 1107 2020, Beirut, Lebanon, Beirut, Lebanon.
3
Centre de Neurophysique, Physiologie et Pathologie, Université Paris Descartes, CNRS UMR 8119, Paris, France.
4
Paris Descartes University, INSERM UMR-S 1124, Faculty of Basic and Biomedical Sciences, 45 rue des Saints-Pères, 75270, Paris Cedex 6, France. charbel.massaad@parisdescartes.fr.

Abstract

Reactive oxygen species (ROS) modify proteins and lipids leading to deleterious outcomes. Thus, maintaining their homeostatic levels is vital. This study highlights the endogenous role of LXRs (LXRα and β) in the regulation of oxidative stress in peripheral nerves. We report that the genetic ablation of both LXR isoforms in mice (LXRdKO) provokes significant locomotor defects correlated with enhanced anion superoxide production, lipid oxidization and protein carbonylation in the sciatic nerves despite the activation of Nrf2-dependant antioxidant response. Interestingly, the reactive oxygen species scavenger N-acetylcysteine counteracts behavioral, electrophysical, ultrastructural and biochemical alterations in LXRdKO mice. Furthermore, Schwann cells in culture pretreated with LXR agonist, TO901317, exhibit improved defenses against oxidative stress generated by tert-butyl hydroperoxide, implying that LXRs play an important role in maintaining the redox homeostasis in the peripheral nervous system. Thus, LXR activation could be a promising strategy to protect from alteration of peripheral myelin resulting from a disturbance of redox homeostasis in Schwann cell.

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