Nrf2 Signaling in Sodium Azide-Treated Oligodendrocytes Restores Mitochondrial Functions

Journal of Molecular Neuroscience : MN
Annette Liessem-SchmitzAthanassios Fragoulis

Abstract

Mitochondrial dysfunctions mark a critical step in many central nervous system (CNS) pathologies, including multiple sclerosis (MS). Such dysfunctions lead to depolarization of mitochondrial membranes and imbalanced redox homeostasis. In this context, reactive oxygen species (ROS) are potentially deleterious but can also act as an important signaling step for cellular maintenance. The transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2), the key regulator in the cellular oxidative stress-response, induces a battery of genes involved in repair and regeneration. Here, we investigated the relevance of Nrf2 signaling for the prevention of cellular damage caused by dysfunctional mitochondria. We employed sodium azide (SA) as mitochondrial inhibitor on oligodendroglial OliNeu cells in vitro, and the cuprizone model with wild type and GFAP-Cre+::Keap1loxP/loxP mice to induce mitochondrial defects. The importance of Nrf2 for cellular functions and survival after SA treatment was elucidated by in vitro knockdown experiments with shRNA directed against Nrf2 and its inhibitor Keap1 as well as by methysticin treatment. Metabolic activity, cytotoxicity, and depolarization of the mitochondrial membrane were analyzed after ...Continue Reading

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Citations

Mar 23, 2021·Cellular and Molecular Life Sciences : CMLS·Jan SpaasTim Vanmierlo

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Methods Mentioned

BETA
Assay
gene array
transfection
flow cytometry
reverse transcription-PCR

Software Mentioned

GraphPad Prism
GraphPad

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