ArticleMedical science monitor : international medical journal of experimental and clinical research2021
lncRNA MEG3 Downregulation Relieves Intracerebral Hemorrhage by Inhibiting Oxidative Stress and Inflammation in an miR-181b-Dependent Manner.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- A Systematic Review of MicroRNAs in Hemorrhagic Neurovascular Disease: Cerebral Cavernous Malformations as a Paradigm.International journal of molecular sciences · 2025Pooled it
- Macrophage migration inhibitory factor alleviates irradiation induced apoptosis of BMSCs through the LncRNA MEG3/NOX4 axis.Open medicine (Warsaw, Poland) · 2026Article
- Electroacupuncture Ameliorates Neuroinflammatory Injury in CPSP Rats by Inhibiting the LncRNA MEG3-Mediated Wnt/β-Catenin Signaling Pathway.Neurochemical research · 2025Article
- From bench to bedside: nanomedicine development for intracerebral hemorrhage - exploring microenvironment, innovation, and translation.Journal of nanobiotechnology · 2025Review
- Regulation of ferroptosis in osteoarthritis and osteoarthritic chondrocytes by typical MicroRNAs in chondrocytes.Frontiers in medicine · 2024Review
- Article
- LncRNA-PEAK1 promotes neuronal apoptosis after intracerebral hemorrhage by miR-466i-5p/caspase 8 axis.Heliyon · 2023Article
- mRNA and lncRNA co-expression network in mice of acute intracerebral hemorrhage.Frontiers in molecular neuroscience · 2023Article
- Long non-coding RNAs in intracerebral hemorrhage.Frontiers in molecular neuroscience · 2023Review
- Macrophage migration inhibitory factor protects bone marrow mesenchymal stem cells from hypoxia/ischemia-induced apoptosis by regulating lncRNA MEG3.Journal of Zhejiang University. Science. B · 2022Article
- Epigenetic mechanisms and potential therapeutic targets in stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Review
- Article
- LncRNA MEG3: Potential stock for precision treatment of cardiovascular diseases.Frontiers in pharmacology · 2022Review
- MicroRNAs modulate neuroinflammation after intracerebral hemorrhage: Prospects for new therapy.Frontiers in immunology · 2022Review
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND This study was designed to illustrate the effects and latent mechanism of lncRNA maternally expressed gene 3 (MEG3) on intracerebral hemorrhage (ICH)-induced brain injury. MATERIAL AND METHODS An ICH rat model was generated to determine the role of lncRNA MEG3 in ICH. The interaction between lncRNA MEG3 and microRNA (miR)-181b were confirmed by Starbase and dual-luciferase reporter assay. One hour (h) or 3 days after ICH stimulation, rat neurological injury was evaluated by modified Neurological Severity Score (mNSS). Brain water content and cell apoptosis were assessed using brain edema assessment and flow cytometry (FCM), respectively. Caspase3 activity was also determined. Enzyme-linked immunosorbent assay (ELISA) was applied to evaluate the levels of pro-inflammatory cytokines. Moreover, the representative biomarkers of oxidative stress were evidenced using detection kits. RESULTS The lncRNA MEG3 level in ICH rat brain tissues was higher than that in the sham group. miR-181b was a direct target of lncRNA MEG3 and it was downregulated in brain tissues of ICH rats. Notably, we found that neurobehavioral scores, brain water content, and neuronal apoptosis were decreased and caspase3 activity was reduced in MEG3-shRNA-treated ICH rats, while we observed the opposite result in ICH+MEG3-shRNA+miR-181b inhibitor rats. Further analyses revealed that MEG3-shRNA inhibited inflammatory cytokines release and reduced oxidative stress. All these results were reversed by miR-181b inhibitor. In addition, MEG3-shRNA activated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway, which was reversed by miR-181b inhibitor. CONCLUSIONS MEG3-shRNA restrained oxidative stress and inflammation following ICH in an miR-181b-dependent manner.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.