Journal of neuroinflammation, 2019-04, Vol.16 (1), p.75-75, Article 75
2019
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- Autor(en) / Beteiligte
- Titel
- LncRNA-1810034E14Rik reduces microglia activation in experimental ischemic stroke
- Ist Teil von
- Journal of neuroinflammation, 2019-04, Vol.16 (1), p.75-75, Article 75
- Ort / Verlag
- England: BioMed Central Ltd
- Erscheinungsjahr
- 2019
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Activation of microglial cells plays an important role in neuroinflammation after ischemic stroke. Inhibiting the activation of microglial cells has been suggested as a potential therapeutic approach in the treatment of ischemic stroke. Oxygen-glucose deprivation in primary microglial cells and transient middle cerebral artery occlusion (MCAO) in C57BL/6 mice were used as the in vitro and in vivo ischemic stroke models. Microarray analysis was performed to investigate the overall impact of long non-coding RNAs (lncRNAs) on the inflammation status of microglial cells. RT-qPCR was used to evaluate the lncRNA levels and mRNA levels of cytokines and microglial cell markers. ELISA was taken to measure the level of cytokines. Immunofluorescence was used to observe the activation of microglial cells. Western blotting was performed to test the p65 phosphorylation. In this study, we showed that LncRNA-1810034E14Rik was significantly decreased in LPS-treated or oxygen-glucose deprivation-induced microglial cells. Overexpression of 1810034E14Rik decreased the infarct volume and alleviated brain damage in MCAO mice. 1810034E14Rik overexpression reduced the expression of inflammatory cytokines not only in ischemic stroke mice but also in oxygen-glucose deprivation-induced microglial cells. Moreover, 1810034E14Rik overexpression could suppress the activation of microglial cells and inhibit the phosphorylation of p65. LncRNA-1810034E14Rik plays an anti-inflammatory role in ischemic stroke and regulates p65 phosphorylation, making it a potential target for stroke treatment.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1742-2094eISSN: 1742-2094DOI: 10.1186/s12974-019-1464-xTitel-ID: cdi_doaj_primary_oai_doaj_org_article_f333710e85704bc4957fb00a96494bad
- Format
- –
- Schlagworte
- Animal models, Animals, Animals, Newborn, Brain injury, Brain research, Care and treatment, Cell Hypoxia - drug effects, Cells, Cultured, Cerebral blood flow, Cytokines, Cytokines - genetics, Cytokines - metabolism, Development and progression, Disease Models, Animal, Enzyme-linked immunosorbent assay, Gene Expression Regulation - drug effects, Gene Expression Regulation - genetics, Genes, Genetic aspects, Glucose, Glucose - deficiency, Health aspects, Immunofluorescence, Infarction, Middle Cerebral Artery - metabolism, Infarction, Middle Cerebral Artery - pathology, Inflammation, Ischemia, Ischemic stroke, Lipopolysaccharides, Lipopolysaccharides - toxicity, lncRNA-1810034E14Rik, Male, Medical prognosis, Mice, Mice, Inbred C57BL, Microarray Analysis, Microglia, Microglia - drug effects, Microglia - metabolism, Microglial cells, mRNA, Non-coding RNA, Oxygen, p65, Phosphoprotein Phosphatases - genetics, Phosphoprotein Phosphatases - metabolism, Phosphorylation, RNA, RNA, Long Noncoding - genetics, RNA, Long Noncoding - metabolism, RNA, Messenger - metabolism, RNA, Small Interfering - pharmacology, Stroke, Stroke (Disease), Transcription Factor RelA - metabolism, Western blotting