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Cited by 530Neuroinflammation and Neurodegeneration MechanismsRedox biology and oxidative stressMitochondrial Function and Pathology

The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.

Mitochondrial ROS govern the LPS-induced pro-inflammatory response in microglia cells by regulating MAPK and NF-κB pathways

Park, Junghyung, Min, Ju-Sik, Kim, Bokyung, Chae, Un-Bin, Yun, Jong Won, Choi, Myung-Sook, Kong, Il-Keun, Chang, Kyu-Tae, Lee, Dong-Seok·2015·Neuroscience Letters
DOI 10.1016/j.neulet.2014.10.016
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Abstract

Activation of microglia cells in the brain contributes to neurodegenerative processes promoted by many neurotoxic factors such as pro-inflammatory cytokines and nitric oxide (NO). Reactive oxygen species (ROS) actively affect microglia-associated neurodegenerative diseases through their role as pro-inflammatory molecules and modulators of pro-inflammatory processes. Although the ROS which involved in microglia activation are thought to be generated primarily by NADPH oxidase (NOX) and involved in the immune response, mitochondrial ROS have also been proposed as important regulators of the inflammatory response in the innate immune system. However, the role of mitochondrial ROS in microglial activation has yet to be fully elucidated. In this study, we demonstrate that inhibition of mitochondrial ROS by treatment with Mito-TEMPO effectively suppressed the level of mitochondrial and intracellular ROS. Mito-TEMPO treatment also significantly prevented LPS-induced increase in the TNF-α, IL-1β, IL-6, iNOS and Cox-2 in BV-2 and primary microglia cells. Furthermore, LPS-induced suppression of mitochondrial ROS generation not only affected LPS-stimulated activation of MAPKs, including ERK, JNK, and p38, but also regulated IκB activation and NF-κB nuclear localization. These results indicate that mitochondria constitute a major source of ROS generation in LPS-mediated activated microglia cells. Additionally, suppression of LPS-induced mitochondrial ROS plays a role in modulating the production of pro-inflammatory mediators by preventing MAPK and NF-κB activation in microglia cells. Our findings suggest that a potential strategy in the development of therapy for inflammation-associated degenerative neurological diseases involves targeting the regulation of mitochondrial ROS in microglial cells.

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Metadata

Authors
Park, J., Min, J.-S., Kim, B., Chae, U.-B., Yun, J. W., Choi, M.-S., Kong, I.-K., Chang, K.-T., & Lee, D.-S.
Affiliations
  • Kyungpook National University (KR)
  • Daegu University (KR)
  • Gyeongsang National University (KR)
  • Korea Research Institute of Bioscience and Biotechnology (KR)
Corresponding author
Lee, Dong-Seok
ORCID
Venue
Neuroscience Letters
Publisher
Elsevier BV
Published
2015-01
Volume
584
Pages
191-196
ISSN
0304-3940 (ISSN-L)
DOI
10.1016/j.neulet.2014.10.016
OpenAlex
W2042183116
Cited by
529
References
26
Citations by year
2026: 53 · 2025: 37 · 2024: 59 · 2023: 64 · 2022: 64 · 2021: 47 · 2020: 51 · 2019: 54 · 2018: 43 · 2017: 23 · 2016: 18 · 2015: 15
FWCI
9.69
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neuroscience Letters (publishedVersion)
  • PubMed (publishedVersion)
  • KRIBB Repository (submittedVersion)
Funders
  • National Research Foundation of Korea (NRF-2012R1A1A2008880, 112020-03-2-SB020)
  • Korea Institute of Planning & Evaluation for Technology in Food, Agriculture, Forestry and Fisheries (2008-0062618)
  • Korea Research Institute of Bioscience and Biotechnology (KGM4611411)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
mitochondrial reactive oxygen species, microglial activation, lipopolysaccharide, pro-inflammatory response, MAPK signaling, NF-κB signaling, MitoTEMPO, ERK, JNK, p38 MAPK, TNF-α, IL-1β, interleukin-6, inducible nitric oxide synthase, cyclooxygenase-2, neuroinflammation, neurodegenerative diseases
MeSH terms
Animals, Cell Line, Inflammation, Lipopolysaccharides, Mitochondria, Organophosphorus Compounds, Piperidines, Signal Transduction, NF-kappa B, Reactive Oxygen Species, Microglia, Mitogen-Activated Protein Kinases, Extracellular Signal-Regulated MAP Kinases, p38 Mitogen-Activated Protein Kinases, MAP Kinase Kinase 4, Mice

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