ArticleJournal of Alzheimer's disease : JAD2018
Inflammatory Cytokine, IL-1β, Regulates Glial Glutamate Transporter via microRNA-181a in vitro.
Article in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- A Systematic Review of MicroRNA Expression as Biomarker of Late-Onset Alzheimer's Disease.Molecular neurobiology · 2019Pooled it
- Effects of MC-100093, GLT-1 enhancer, in mesolimbic brain regions of C57BL/6 mouse exposed to hydrocodone high-dose challenge using comprehensive laboratory monitoring system.IBRO neuroscience reports · 2026Article
- The neuroimmune-glutamate hypothesis of addiction.Neuroscience and biobehavioral reviews · 2026Review
- The Glutamate-Glutathione axis in neuropsychiatric disorders and cancer: From shared mechanisms to non-invasive biomarkers.Redox biology · 2026Review
- Impairment of hippocampal long-term potentiation by soluble amyloid-β oligomers is mediated by glutamate transporter 1 expressed in neurons.Neural regeneration research · 2026Article
- Alzheimer's Disease as a Disorder of Neuroimmune Dysregulation.Neurology international · 2026Review
- Exercise-derived extracellular vesicles in oncology: a new frontier for translational nanomedicine.Journal of translational medicine · 2026Review
- The Role of Exercise in Regulating the Generation of Extracellular Vesicles in Cardiovascular Diseases.Reviews in cardiovascular medicine · 2024Review
- Microglia in neuroimmunopharmacology and drug addiction.Molecular psychiatry · 2024Review
- Extracellular Vesicles in the Central Nervous System: A Novel Mechanism of Neuronal Cell Communication.International journal of molecular sciences · 2024Review
- Pathophysiology to Risk Factor and Therapeutics to Treatment Strategies on Epilepsy.Brain sciences · 2024Review
- Regulation of Glial Function by Noncoding RNA in Central Nervous System Disease.Neuroscience bulletin · 2023Review
- Article
- Analgesic Alkaloids Derived From Traditional Chinese Medicine in Pain Management.Frontiers in pharmacology · 2022Review
- MiR-27a-3p and miR-30b-5p inhibited-vitamin D receptor involved in the progression of tuberculosis.Frontiers in microbiology · 2022Article
- Neuroinflammation, Sleep, and Circadian Rhythms.Frontiers in cellular and infection microbiology · 2022Review
- Involvement of Astrocytes and microRNA Dysregulation in Neurodegenerative Diseases: From Pathogenesis to Therapeutic Potential.Frontiers in molecular neuroscience · 2021Article
- The formative role of microglia in stress-induced synaptic deficits and associated behavioral consequences.Neuroscience letters · 2019Review
- Microglia in Alzheimer's Disease: Risk Factors and Inflammation.Frontiers in neurology · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Glutamate overload triggers synaptic and neuronal loss that potentially contributes to neurodegenerative diseases including Alzheimer's disease (AD). Glutamate clearance and regulation at synaptic clefts is primarily mediated by glial glutamate transporter 1 (GLT-1). We determined that inflammatory cytokines significantly upregulated GLT-1 through microRNA-181a-mediated post-transcriptional modifications. Unveiling the key underlying mechanisms modulating GLT-1 helps better understand its physiological and pathological interactions with cytokines. Primary murine astrocyte and neuron co-culture received 20 ng/mL IL-1β, TNF-α, or IL-6 for 48 h. Soluble proteins or total RNA were extracted after treatment for further analyses. Treatment with inflammatory cytokines, IL-1β and TNF-α, but not IL-6, significantly increased GLT-1 steady-state levels (p≤0.05) without affecting mRNA levels, suggesting the cytokine-induced GLT-1 was regulated through post-transcriptional modifications. Among the candidate microRNAs predicted to modulate GLT-1, only microRNA-181a was significantly decreased following the IL-1β treatment (p≤0.05). Co-treatment of microRNA-181a mimic in IL-1β-treated primary astrocytes and neurons effectively blocked the IL-1β-induced upregulation of GLT-1. Lastly, we attempted to determine the link between GLT-1 and microRNA-181a in human AD brains. A significant reduction of GLT-1 was found in AD hippocampus tissues, and the ratio of mature microRNA-181a over primary microRNA-181a had an increasing tendency in AD. MicroRNA-181a controls rapid modifications of GLT-1 levels in astrocytes. Cytokine-induced inhibition of microRNA-181a and subsequent upregulation of GLT-1 may have physiological implications in synaptic plasticity while aberrant maturation of microRNA-181a may be involved in pathological consequences in AD.
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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.