ArticleJournal of molecular neuroscience : MN2021
LncRNA HOTAIR Participates in Microglia Activation and Inflammatory Factor Release by Regulating the Ubiquitination of MYD88 in Traumatic Brain Injury.
Article in Journal of molecular neuroscience : MN, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 41 citations in OpenAlex.
- RNA-binding proteins: a comprehensive review of multifaceted regulatory mechanisms in neuroinflammation and implications in the pathogenesis of neurological disorders.Journal of neuroinflammation · 2026Review
- EV-associated HOTAIR in cancer cell communication: a distance-aware review of functional transfer claims.Frontiers in cell and developmental biology · 2026Review
- Progenitor cells, microglia, and non-coding RNAs: Orchestrators of glioblastoma pathogenesis and therapeutic resistance.Non-coding RNA research · 2025Review
- LncRNA levels in the central nervous system as novel potential players and biomarkers in amyotrophic lateral sclerosis.Non-coding RNA research · 2025Article
- 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
- The Role of Long Non-Coding RNA in Anxiety Disorders: A Literature Review.International journal of molecular sciences · 2025Review
- LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.Cellular and molecular neurobiology · 2025Review
- Comprehensive Transcriptome-Wide Profiling of 5-Methylcytosine Modifications in Long Non-Coding RNAs in a Rat Model of Traumatic Brain Injury.Current issues in molecular biology · 2024Article
- LncRNA ILF3-AS1 mediates oxidative stress and inflammation through miR-504-3p/HMGB1 axis in a cellular model of temporal lobe epilepsy.Brain and behavior · 2024Article
- The multifaceted functions of long non-coding RNAExpert reviews in molecular medicine · 2024Review
- Roles of HOTAIR Long Non-coding RNA in Gliomas and Other CNS Disorders.Cellular and molecular neurobiology · 2024Review
- Long Noncoding RNA VLDLR-AS1 Levels in Serum Correlate with Combat-Related Chronic Mild Traumatic Brain Injury and Depression Symptoms in US Veterans.International journal of molecular sciences · 2024Article
- Extracellular vesicles as carriers for noncoding RNA-based regulation of macrophage/microglia polarization: an emerging candidate regulator for lung and traumatic brain injuries.Frontiers in immunology · 2024Review
- Role of regulatory non-coding RNAs in traumatic brain injury.Neurochemistry international · 2024Review
- β-Sitosterol Alleviates Neuropathic Pain by Affect Microglia Polarization through Inhibiting TLR4/NF-κB Signaling Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Article
- Emerging role of non-coding RNAs in neuroinflammation mediated by microglia and astrocytes.Journal of neuroinflammation · 2023Review
- Regulation of Glial Function by Noncoding RNA in Central Nervous System Disease.Neuroscience bulletin · 2023Review
- Non-Coding RNA in Microglia Activation and Neuroinflammation in Alzheimer's Disease.Journal of inflammation research · 2023Review
- TAK-242, a toll-like receptor 4 antagonist, against brain injury by alleviates autophagy and inflammation in rats.Open life sciences · 2023Article
- Role of primary aging hallmarks in Alzheimer´s disease.Theranostics · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is one of the leading causes of death worldwide. Long non-coding RNAs (LncRNAs) have been reported to be closely associated with various diseases, but their roles in TBI has not been fully elucidated. The purpose of this study was to elucidate the underlying mechanism of LncRNA HOTAIR in TBI-induced microglial activation and inflammatory factor release. In vivo mouse TBI model and in vitro microglia activation model were established by Feeney's free-fall impact method and by LPS stimulation, respectively. The expression of LncRNA HOTAIR in activated microglia was detected by qRT-PCR. After shRNA knocked down, the expressions of LncRNA HOTAIR and microglia activation marker Iba-1 in microglia were detected by qRT-PCR and Western blot and by ELISA that detected the concentration of inflammatory factor in cell culture supernatants. The relationship between LncRNA HOTAIR and MYD88 in mouse microglia BV2 cells was observed by RNA pull-down assay. Furthermore, the effect of LncRNA HOTAIR on MYD88 stability was assessed by cycloheximide (CHX)-chase and by immunoprecipitation and ubiquitination assays that analyzed MYD88 ubiquitination. LncRNA HOTAIR was abnormally highly expressed in activated microglia. By Western blot and ELISA, the knockdown of LncRNA HOTAIR in microglia significantly repressed microglia activation and inflammatory factor release. By RNA pull-down assay, LncRNA HOTAIR could bind to MYD88 protein. Besides, by cycloheximide (CHX)-chase and immunoprecipitation and ubiquitination assays, the overexpression of the LncRNA HOTAIR enhanced the stability of MYD88 protein and inhibited Nrdp1-mediated ubiquitination of MYD88 protein. After the transfection of shRNA-HOTAIR and shRNA-HOTAIR+pcDNA-MYD88 into microglia, shRNA-HOTAIR could significantly inhibit the activation of microglia and the release of inflammatory factors, while these effects were reversed after the transfection of pcDNA-MYD88. Our experimental data indicated that LncRNA HOTAIR was highly expressed in activated microglia, and our further studies had found that the interference with LncRNA HOTAIR could repress microglia activation and inflammatory factor release via promoting Nrdp1-mediated ubiquitination of MYD88 protein.
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