Abstract |
The retinoic acid-inducible gene I (RIG-I) is a crucial cytoplasmic pathogen recognition receptor involved in neuroinflammation in degenerative diseases. In the present study, in vitro human astrocytes were subjected to a chemical hypoxia model using cobalt chloride pretreatment. Chemical hypoxia induces the up-regulation of RIG-I in astrocytes and results in the expression of inflammatory cytokines IL-1β, IL-6, and TNF-α in an NF-κB dependent manner. Elevated RIG-I modulates the interaction of interferon-β promoter stimulator-1 (IPS-1) and TNF receptor-associated factor 6 ( TRAF6) following chemical hypoxia. Inhibition of IPS-1 or TRAF6 suppresses RIG-I-induced NF-κB activation and inflammatory cytokines in response to chemical hypoxia. These data suggest that chemical hypoxia leads to RIG-I activation and the expression of inflammatory cytokines through the NF-κB pathway. Blocking IPS-1/ TRAF6 pathway relieves RIG-I-induced neuroinflammation in astrocytes subjected to hypoxia.
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Authors | Lei Li, Rongli Yang, Meijiang Feng, YiChen Guo, YuXuan Wang, Jun Guo, Xiang Lu |
Journal | Neuroscience letters
(Neurosci Lett)
Vol. 672
Pg. 46-52
(04 13 2018)
ISSN: 1872-7972 [Electronic] Ireland |
PMID | 29474875
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2018 Elsevier B.V. All rights reserved. |
Chemical References |
- Adaptor Proteins, Signal Transducing
- MAVS protein, human
- Receptors, Immunologic
- TNF Receptor-Associated Factor 6
- Cobalt
- DDX58 protein, human
- DEAD Box Protein 58
- cobaltous chloride
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Topics |
- Adaptor Proteins, Signal Transducing
(metabolism)
- Astrocytes
(drug effects, metabolism)
- Cell Hypoxia
(drug effects, physiology)
- Cell Line, Tumor
- Cobalt
(pharmacology)
- DEAD Box Protein 58
(metabolism)
- Humans
- Inflammation
(metabolism)
- Receptors, Immunologic
- Signal Transduction
(drug effects)
- TNF Receptor-Associated Factor 6
(metabolism)
- Up-Regulation
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