Abstract |
Cerebral ischemia occurs when blood flow to part of the brain is obstructed, which can result in oxygen and glucose deprivation (OGD) and neuronal damage. However, the mechanisms remain poorly understood. The present study investigated the production and effects of double-stranded RNA (dsRNA) induced by OGD in neuronal cells. By confocal microscopy, dsRNA containing B1 and B2 RNA, was found accumulating in HT22 cells under OGD treatment. The sequence of B1 RNA was identified and transfected into HT22 cells. Interestingly, B1 RNA induced transcription and expression of NLRP3, interleukin (IL)-1β, and tumor necrosis factor (TNF)-α, which was similar to the effects of OGD treatment. Moreover, HT22 cell growth inhibition and proinflammatory cytokines production induced by OGD and B1 RNA treatment were down-regulated by NLRP3 knock-down. These findings suggest that B1 RNA induced by OGD forms as dsRNA and inhibits neuronal cell metabolic activity by regulating the NLRP3 and associated proinflammatory cytokines production.
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Authors | Li Wang, Weihua Wang, Lei Zhang, Peng Dai, Kai Wang, Hao Hui, Wei Rao, Cheng Peng, Jinghua Yang, Zhen Yan, Zhou Fei |
Journal | Neuroscience letters
(Neurosci Lett)
Vol. 588
Pg. 147-53
(Feb 19 2015)
ISSN: 1872-7972 [Electronic] Ireland |
PMID | 25543031
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. |
Chemical References |
- Carrier Proteins
- Interleukin-1beta
- NLR Family, Pyrin Domain-Containing 3 Protein
- Nlrp3 protein, mouse
- RNA, Double-Stranded
- Retroelements
- Tumor Necrosis Factor-alpha
- RNA
- Glucose
- Oxygen
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Topics |
- Animals
- Carrier Proteins
(genetics, metabolism)
- Cells, Cultured
- Glucose
(deficiency)
- Infarction, Middle Cerebral Artery
(pathology)
- Interleukin-1beta
(biosynthesis, genetics)
- Mice, Inbred BALB C
- NLR Family, Pyrin Domain-Containing 3 Protein
- Neurons
(pathology)
- Oxygen
(metabolism)
- Plasmids
- RNA
(genetics)
- RNA, Double-Stranded
(genetics)
- Retroelements
- Tumor Necrosis Factor-alpha
(biosynthesis, genetics)
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