ArticleCell death and differentiation2016
miR-711 upregulation induces neuronal cell death after traumatic brain injury.
Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 72 citations in OpenAlex.
- Mechanistically informed circulating biomarkers are associated with acquired epilepsy after neonatal brain injury.Journal of neuroinflammation · 2026Observational
- Unveiling the predictive power of biomarkers in traumatic brain injury: A narrative review focused on clinical outcomes.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2025Review
- Mitophagy in intracerebral hemorrhage: a new target for therapeutic intervention.Neural regeneration research · 2024Review
- Study on serum miR-185-5p in assessing the injury severity and prognosis of patients with traumatic brain injury.Journal of medical biochemistry · 2023Article
- Micro RNAs as a Diagnostic Marker between Glioma and Primary CNS Lymphoma: A Systematic Review.Cancers · 2023Review
- Non-coding RNAs and Exosomal Non-coding RNAs in Traumatic Brain Injury: the Small Player with Big Actions.Molecular neurobiology · 2023Review
- Potential application of let-7a antagomir in injured peripheral nerve regeneration.Neural regeneration research · 2023Article
- Adiponectin reduces apoptosis of diabetic cardiomyocytes by regulating miR-711/TLR4 axis.Diabetology & metabolic syndrome · 2022Article
- Review
- Article
- Rescuing mitochondria in traumatic brain injury and intracerebral hemorrhages - A potential therapeutic approach.Neurochemistry international · 2021Review
- Heat stress induced arginylation of HuR promotes alternative polyadenylation of Hsp70.3 by regulating HuR stability and RNA binding.Cell death and differentiation · 2021Article
- Article
- Peering into the Brain through the Retrosplenial Cortex to Assess Cognitive Function of the Injured Brain.Neurotrauma reports · 2021Article
- Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions.Biomedicines · 2020Review
- Mithramycin selectively attenuates DNA-damage-induced neuronal cell death.Cell death & disease · 2020Article
- Irradiation-Induced Upregulation of miR-711 Inhibits DNA Repair and Promotes Neurodegeneration Pathways.International journal of molecular sciences · 2020Article
- microRNA-9-5p alleviates blood-brain barrier damage and neuroinflammation after traumatic brain injury.Journal of neurochemistry · 2020Article
- Down-Regulation of miR-23a-3p Mediates Irradiation-Induced Neuronal Apoptosis.International journal of molecular sciences · 2020Article
- Role of circular RNAs in brain development and CNS diseases.Progress in neurobiology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is a leading cause of mortality and disability. MicroRNAs (miRs) are small noncoding RNAs that negatively regulate gene expression at post-transcriptional level and may be key modulators of neuronal apoptosis, yet their role in secondary injury after TBI remains largely unexplored. Changes in miRs after controlled cortical impact (CCI) in mice were examined during the first 72 h using miR arrays and qPCR. One selected miR (711) was examined with regard to its regulation and relation to cell death; effects of miR-711 modulation were evaluated after CCI and using in vitro cell death models of primary cortical neurons. Levels of miR-711 were increased in the cortex early after TBI and in vitro models through rapid upregulation of miR-711 transcription (pri-miR-711) rather than catabolism. Increases coincided with downregulation of the pro-survival protein Akt, a predicted target of miR-711, with sequential activation of forkhead box O3 (FoxO3)a/glycogen synthase kinase 3 (GSK3)α/β, pro-apoptotic BH3-only molecules PUMA (Bcl2-binding component 3) and Bim (Bcl2-like 11 (apoptosis facilitator)), and mitochondrial release of cytochrome c and AIF. miR-711 and Akt (mRNA) co-immunoprecipitated with the RNA-induced silencing complex (RISC). A miR-711 hairpin inhibitor attenuated the apoptotic mechanisms and decreased neuronal death in an Akt-dependent manner. Conversely, a miR-711 mimic enhanced neuronal apoptosis. Central administration of the miR-711 hairpin inhibitor after TBI increased Akt expression and attenuated apoptotic pathways. Treatment reduced cortical lesion volume, neuronal cell loss in cortex and hippocampus, and long-term neurological dysfunction. miR-711 changes contribute to neuronal cell death after TBI, in part by inhibiting Akt, and may serve as a novel therapeutic target.
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