| Title |
Nrf2 Signaling in Sodium Azide-Treated Oligodendrocytes Restores Mitochondrial Functions
|
|---|---|
| Published in |
Journal of Molecular Neuroscience, August 2018
|
| DOI | 10.1007/s12031-018-1159-2 |
| Pubmed ID | |
| Authors |
Annette Liessem-Schmitz, Nico Teske, Miriam Scheld, Stella Nyamoya, Adib Zendedel, Cordian Beyer, Tim Clarner, Athanassios 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 SA treatment. The expression of Nrf2 target genes as well as endoplasmic reticulum stress response genes was additionally measured by real-time PCR (in vitro) and PCR gene arrays (in vivo). Treatment of OliNeu cells with SA resulted in significant depolarization of the mitochondrial membrane, decreased metabolic activity, and increased cytotoxicity. This was partly counteracted in Nrf2-hyperactivated cells and intensified in Nrf2-knockdown cells. Our studies demonstrate a key role of Nrf2 in maintaining cellular functions and survival in the context of mitochondrial dysfunction. |
X Demographics
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Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Australia | 1 | 50% |
| Unknown | 1 | 50% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 2 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 22 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 22 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Bachelor | 3 | 14% |
| Student > Ph. D. Student | 3 | 14% |
| Student > Doctoral Student | 2 | 9% |
| Researcher | 2 | 9% |
| Lecturer | 1 | 5% |
| Other | 4 | 18% |
| Unknown | 7 | 32% |
| Readers by discipline | Count | As % |
|---|---|---|
| Neuroscience | 4 | 18% |
| Agricultural and Biological Sciences | 3 | 14% |
| Medicine and Dentistry | 2 | 9% |
| Chemical Engineering | 1 | 5% |
| Nursing and Health Professions | 1 | 5% |
| Other | 3 | 14% |
| Unknown | 8 | 36% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 25 August 2018.
All research outputs
#20,663,600
of 25,385,509 outputs
Outputs from Journal of Molecular Neuroscience
#1,156
of 1,643 outputs
Outputs of similar age
#266,386
of 342,525 outputs
Outputs of similar age from Journal of Molecular Neuroscience
#25
of 46 outputs
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