ArticleIn vitro cellular & developmental biology. Animal2019
YY1-induced upregulation of lncRNA NEAT1 contributes to OGD/R injury-induced inflammatory response in cerebral microglial cells via Wnt/β-catenin signaling pathway.
Article in In vitro cellular & developmental biology. Animal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- A systematic review of the research progress of non-coding RNA in neuroinflammation and immune regulation in cerebral infarction/ischemia-reperfusion injury.Frontiers in immunology · 2022Pooled it
- Defining the transcriptional routes controlling lncRNA NEAT1 expression: implications in cellular stress response, inflammation, and differentiation.Discover oncology · 2025Review
- Gastrodin: a potential natural product for the prevention and treatment of cerebral ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- Brain alarm by self-extracellular nucleic acids: from neuroinflammation to neurodegeneration.Journal of biomedical science · 2023Review
- Non-Coding RNA in Microglia Activation and Neuroinflammation in Alzheimer's Disease.Journal of inflammation research · 2023Review
- Long non-coding RNAs as biomarkers and therapeutic targets for ischemic stroke.Non-coding RNA research · 2022Review
- The Emerging Roles of Long Non-Coding RNAs in Intellectual Disability and Related Neurodevelopmental Disorders.International journal of molecular sciences · 2022Review
- Characterization of Ex Vivo and In Vitro Wnt Transcriptome Induced by Spinal Cord Injury in Rat Microglial Cells.Brain sciences · 2022Article
- LncRNA NEAT1 ameliorate ischemic stroke via promoting Mfn2 expression through binding to Nova and activates Sirt3.Metabolic brain disease · 2022Article
- Article
- Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation.Journal of inflammation research · 2022Review
- Non-Coding RNAs as Novel Regulators of Neuroinflammation in Alzheimer's Disease.Frontiers in immunology · 2022Review
- Identification of programmed cell death-related gene signature and associated regulatory axis in cerebral ischemia/reperfusion injury.Frontiers in genetics · 2022Article
- Bioinformatics analysis andFrontiers in pharmacology · 2022Article
- Gastrodin Alleviates Cerebral Ischaemia/Reperfusion Injury by Inhibiting Pyroptosis by Regulating the lncRNA NEAT1/miR-22-3p Axis.Neurochemical research · 2021Article
- Non-Syndromic Intellectual Disability and Its Pathways: A Long Noncoding RNA Perspective.Non-coding RNA · 2021Review
- Knockdown lncRNA NEAT1 regulates the activation of microglia and reduces AKT signaling and neuronal apoptosis after cerebral ischemic reperfusion.Scientific reports · 2020Article
- Long non-coding RNA NEAT1-centric gene regulation.Cellular and molecular life sciences : CMLS · 2020Review
- Long noncoding RNA NEAT1 correlates with higher disease risk, worse disease condition, decreased miR-124 and miR-125a and predicts poor recurrence-free survival of acute ischemic stroke.Journal of clinical laboratory analysis · 2020Article
- Microglia and Wnt Pathways: Prospects for Inflammation in Alzheimer's Disease.Frontiers in aging neuroscience · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stroke can lead to the serious long-term neurological disability. The dysregulation of long non-coding RNAs (lncRNAs) has been proven to be a pivotal factor for the progression of ischemic stroke. However, it is largely unknown whether lncRNAs regulated the OGD/R injury of cerebral microglial cells. In this study, we designed experiments to reveal the role of lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) in the OGD/R injury of microglial cells. We found that NEAT1 contributed to the OGD/R injury and neuroinflammation damage in microglial cells. Moreover, the molecular mechanism involved in the NEAT1-mediated OGD/R injury. Mechanism investigation revealed that NEAT1 was upregulated by the transcription factor YY1. Moreover, Western blot analysis suggested that NEAT1 enhance the protein levels of core factors of Wnt/β-catenin signaling pathway, indicating that NEAT1 contributed to the activation of Wnt/β-catenin signaling pathway. Rescue assays were carried out in the microglial cells treated with OGD/R. The results showed that NEAT1 regulated the OGD/R injury and neuroinflammation damage via Wnt/β-catenin signaling pathway. In conclusion, our findings suggested that YY1-induced upregulation of NEAT1 contributed to the OGD/R injury and neuroinflammation damage of microglial cells via Wnt/β-catenin signaling pathway.
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