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

doi:10.1016/j.neulet.2014.10.016

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

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 +1 more·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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Mitochondrial ROS (mROS), independent of NOX-generated ROS, are involved in the inflammatory response of microglia by activating MAPKs.
“Mitochondrial ROS (mROS), independent of NOX-generated ROS, are also involved in the inflammatory response of microglia by activating MAPKs.”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [158]
MAPK and NFκB activation in microglial cells and concurrent upregulation of pro-inflammatory mediators is facilitated, at least in part, by mROS.
“Therefore, MAPK and NFκB activation in microglial cells and the concurrent upregulation of pro-inflammatory mediators is facilitated, at least in part, by mROS.”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [158]

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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: Park, Junghyung
Min, Ju-Sik
Kim, Bokyung
Yun, Jong Won
Choi, Myung-Sook
Kong, Il-Keun
Chang, Kyu-Tae
Lee, Dong-Seok
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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Mitochondrial ROS govern the LPS-induced pro-inflammatory response in microglia cells by regulating MAPK and NF-κB pathways

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