ArticleCell cycle (Georgetown, Tex.)2019
LncRNA MIAT overexpression reduced neuron apoptosis in a neonatal rat model of hypoxic-ischemic injury through miR-211/GDNF.
Article in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Bridging development and disease: the potential of LncRNAs as biomarkers and therapeutics in pediatric neurological disorders.Pediatric research · 2026Review
- Long Non-Coding RNA PVT1 Inhibits Apoptosis Through the miR-30d-5p/CaMKIIδ Axis in Hypoxic-Ischemic Brain Injury.Molecular neurobiology · 2025Article
- Techniques for investigating lncRNA transcript functions in neurodevelopment.Molecular psychiatry · 2024Review
- lncRNA-MIAT rs9625066 polymorphism could be a potential biomarker for ischemic stroke.BMC medical genomics · 2024Article
- Hidden regulators: the emerging roles of lncRNAs in brain development and disease.Frontiers in neuroscience · 2024Review
- LncRNAs and CircRNAs as Strategies against Pathological Conditions Caused by a Hypoxic/Anoxic State.Biomolecules · 2023Review
- What has single-cell transcriptomics taught us about long non-coding RNAs in the ventricular-subventricular zone?Stem cell reports · 2023Article
- LncRNA SNHG15 regulates hypoxic-ischemic brain injury via miR-153-3p/SETD7 axis.Histology and histopathology · 2022Article
- LncRNA MIAT Promotes Spinal Cord Injury Recovery in Rats by Regulating RBFOX2-Mediated Alternative Splicing of MCL-1.Molecular neurobiology · 2022Article
- LncRNA BIRF Promotes Brain Ischemic Tolerance Induced By Cerebral Ischemic Preconditioning Through Upregulating GLT-1 via Sponging miR-330-5p.Molecular neurobiology · 2022Article
- Evaluating the Role of lncRNAs in the Incidence of Cardiovascular Diseases in Androgenetic Alopecia Patients.Cardiovascular toxicology · 2022Review
- An update on the functional roles of long non‑coding RNAs in ischemic injury (Review).International journal of molecular medicine · 2022Review
- Article
- Expression of BDNF-Associated lncRNAs in Parkinson's disease.Metabolic brain disease · 2022Article
- Downregulation of oxytocin-related genes in periodontitis.Frontiers in molecular neuroscience · 2022Article
- LncRNA MIAT Inhibits MPPNeurochemical research · 2021Article
- Long non-coding RNA LOC366613 alleviates the cerebral ischemic injury via regulating the miR-532-5p/phosphatase and tensin homolog axis.Bioengineered · 2021Article
- An Emerging Role for Epigenetics in Cerebral Palsy.Journal of personalized medicine · 2021Review
- Non-Syndromic Intellectual Disability and Its Pathways: A Long Noncoding RNA Perspective.Non-coding RNA · 2021Review
- Non-Coding RNAs Participate in the Pathogenesis of Neuroblastoma.Frontiers in oncology · 2021Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the underlying mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in hypoxic-ischemic (HI)-induced neonatal cerebral palsy. MATERIALS AND
methodsNeonatal rat model of HI injury was established to detect the motor function. LncRNA MIAT, miR-211, glial cell line-derived neurotrophic factor (GDNF) and caspase-3 expressions were measured by qRT-PCR or western blot. The apoptosis of Neuro2A cells was detected by flow cytometry. RNA immunoprecipitation (RIP) and RNA pull-down assays were performed to confirm the interaction between MIAT and miR-211.
resultsCompared with control group, lncRNA MIAT and GDNF were downregulated in striatal tissues of neonatal rats in HI group and oxygen glucose deprivation (OGD)-induced ischemic injury of Neuro2A cells, whereas miR-211 was up-regulated in striatal tissues of HI group and OGD-induced ischemic injury of Neuro2A cells. LncRNA MIAT interacted with miR-211, and lncRNA MIAT overexpression reduced neuron apoptosis through miR-211. Besides, GDNF expression was positively regulated by lncRNA MIAT and negatively regulated by miR-211 in Neuro2A cells. In vivo experiment proved MIAT promoted motor function and relieved HI injury.
conclusionMIAT overexpression reduced apoptosis of Neuro2A cells through miR-211/GDNF, which relieved HI injury of neonatal rats.
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