ArticleNeurotoxicity research2022
Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis.
Article in Neurotoxicity research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Circulating IncRNAs and Their Association With Ischemic Stroke Severity and Prognosis: A Systematic Review and Meta-Analysis.Health science reports · 2026Review
- Human Blood-Derived lncRNAs in Autism Spectrum Disorder.Biomolecules · 2025Review
- The significance of calcium ions in cerebral ischemia-reperfusion injury: mechanisms and intervention strategies.Frontiers in molecular biosciences · 2025Review
- The role of long noncoding ribonucleic acids in the central nervous system injury.Molecular and cellular biochemistry · 2024Review
- LncRNA Tug1 relieves the steatosis of SelenoF-knockout hepatocytes via sponging miR-1934-3p.Cell biology and toxicology · 2023Article
- Review
- The Role of microRNAs in Epigenetic Regulation of Signaling Pathways in Neurological Pathologies.International journal of molecular sciences · 2023Review
- Cognitive Impairment in Multiple Sclerosis.Bioengineering (Basel, Switzerland) · 2023Review
- The forkhead box O3 (FOXO3): a key player in the regulation of ischemia and reperfusion injury.Cellular and molecular life sciences : CMLS · 2023Review
- The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk.Frontiers in immunology · 2023Review
- The Metabolic Basis for Nervous System Dysfunction in Alzheimer's Disease, Parkinson's Disease, and Huntington's Disease.Current neurovascular research · 2023Article
- An update on the functional roles of long non‑coding RNAs in ischemic injury (Review).International journal of molecular medicine · 2022Review
- Protocatechualdehyde Rescues Oxygen-Glucose Deprivation/Reoxygenation-Induced Endothelial Cells Injury by Inducing Autophagy and Inhibiting ApoptosisFrontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Emerging studies illustrate that long non-coding RNA TUG1 (TUG1) participates in neuron death after ischemia. However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p (miR-410), and forkhead box O3 (FOXO3) was detected by RT-qPCR and western blot. Neural function, apoptosis, and inflammatory damage were assessed by triphenyltetrazolium chloride straining, modified neurological severity score, fluorescence-activated cell sorting method, and western blot. The relationship among TUG1, miR-410, and FOXO3 was identified by dual-luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation. Results TUG1 was upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-induced mouse brain microvascular endothelial cells (BMECs) in a certain of time-dependent manner. Blockage of TUG1 decreased infarct volume and increased neurological score in MCAO/R mice, accompanied with elevated Bcl-2 expression and declined expression of IL-1β, IL-6, TNF-α, Bax, and cleaved caspase 3. Abovementioned proteins were similarly expressed in OGD/R-induced BMECs with TUG1 knockdown, paralleled with diminished apoptosis rate. Either, miR-410 overexpression and FOXO3 interference could suppress OGD/R-induced inflammatory and apoptotic responses. Of note, TUG1 and FOXO3 are competing endogenous RNAs (ceRNAs) for miR-410 via target binding. Depleting miR-410 counteracted the role of TUG1 exhaustion, and reinforcing FOXO3 abated the effect of miR-410 overexpression. Conclusion Exhausting TUG1 could alleviate CI/R-induced inflammatory injury and apoptosis in brain tissues and BMECs via targeting miR-410/FOXO3 axis, suggesting an innovative perspective from cerebrovascular endothelial cells in the pathogenesis and treatment of CI/R.
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