ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2019
Inhibition of miR-155 Limits Neuroinflammation and Improves Functional Recovery After Experimental Traumatic Brain Injury in Mice.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 77 citations in OpenAlex.
- The role of microRNAs in executive functions: a comprehensive review and bioinformatics analysis of human and animal studies.Molecular psychiatry · 2026Review
- Microglial TLR7 contributes to traumatic brain injury-induced neuroinflammation in mice.Acta pharmacologica Sinica · 2026Article
- Role of microRNAs in major brain diseases, focusing on neuroinflammation and neuronal apoptosis.Iranian journal of basic medical sciences · 2026Review
- 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
- Emerging targets and translational challenges in treating paclitaxel-induced peripheral neuropathy.Molecular biology reports · 2025Review
- The Application of MicroRNAs in Traumatic Brain Injury: Mechanism Elucidation and Clinical Translation.Molecular neurobiology · 2025Review
- Transforaminal Epidural Steroid Injection in Lumbar Disc Prolapse: Impact on Pain Intensity and Cognitive Function in Relation to MicroRNA-155 Serum Level.Anesthesiology research and practice · 2025Article
- Analysis of miRNA Expression Profiles in Traumatic Brain Injury (TBI) and Their Correlation with Survival and Severity of Injury.International journal of molecular sciences · 2024Article
- Loss of microRNA-15a/16-1 function promotes neuropathological and functional recovery in experimental traumatic brain injury.JCI insight · 2024Article
- Interaction of high-fat diet and brain trauma alters adipose tissue macrophages and brain microglia associated with exacerbated cognitive dysfunction.Journal of neuroinflammation · 2024Article
- Role of microRNAs in cognitive decline related to COVID‑19 (Review).Experimental and therapeutic medicine · 2024Review
- Role of regulatory non-coding RNAs in traumatic brain injury.Neurochemistry international · 2024Review
- Alterations in Serum miR-126-3p Levels over Time: A Marker of Pituitary Insufficiency following Head Trauma.Neuroendocrinology · 2024Article
- Emerging role of non-coding RNAs in neuroinflammation mediated by microglia and astrocytes.Journal of neuroinflammation · 2023Review
- Pathogenesis of miR-155 on nonmodifiable and modifiable risk factors in Alzheimer's disease.Alzheimer's research & therapy · 2023Review
- Recent advances in the role of miRNAs in post-traumatic stress disorder and traumatic brain injury.Molecular psychiatry · 2023Review
- Roles of the miR-155 in Neuroinflammation and Neurological Disorders: A Potent Biological and Therapeutic Target.Cellular and molecular neurobiology · 2023Review
- miR-506-3p Relieves Neuropathic Pain following Brachial Plexus Avulsion via Mitigating Microglial Activation through Targeting the CCL2-CCR2 Axis.Developmental neuroscience · 2023Article
- Enhancing arginase 2 expression using target site blockers as a strategy to modulate macrophage phenotype.Molecular therapy. Nucleic acids · 2022Article
- Upregulation of Spinal miR-155-5p Contributes to Mechanical Hyperalgesia by Promoting Inflammatory Activation of Microglia in Bone Cancer Pain Rats.Life (Basel, Switzerland) · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Micro-RNAs (miRs) are short, noncoding RNAs that negatively regulate gene expression at the post-transcriptional level and have been implicated in the pathophysiology of secondary damage after traumatic brain injury (TBI). Among miRs linked to inflammation, miR-155 has been implicated as a pro-inflammatory factor in a variety of organ systems. We examined the expression profile of miR-155, following experimental TBI (controlled cortical impact) in adult male C57Bl/6 mice, as well as the effects of acute or delayed administration of a miR-155 antagomir on post-traumatic neuroinflammatory responses and neurological recovery. Trauma robustly increased miR-155 expression in the injured cortex over 7 days. Similar TBI-induced miR-155 expression changes were also found in microglia/macrophages isolated from the injured cortex at 7 days post-injury. A miR-155 hairpin inhibitor (antagomir; 0.5 nmol), administered intracerebroventricularly (ICV) immediately after injury, attenuated neuroinflammatory markers at both 1 day and 7 days post-injury and reduced impairments in spatial working memory. Delayed ICV infusion of the miR-155 antagomir (0.5 nmol/day), beginning 24 h post-injury and continuing for 6 days, attenuated neuroinflammatory markers at 7 days post-injury and improved motor, but not cognitive, function through 28 days. The latter treatment limited NADPH oxidase 2 expression changes in microglia/macrophages in the injured cortex and reduced cortical lesion volume. In summary, TBI causes a robust and persistent neuroinflammatory response that is associated with increased miR-155 expression in microglia/macrophages, and miR-155 inhibition reduces post-traumatic neuroinflammatory responses and improves neurological recovery. Thus, miR-155 may be a therapeutic target for TBI-related neuroinflammation.
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