ArticleFrontiers in immunology2018
Experimental Demyelination and Axonal Loss Are Reduced in MicroRNA-146a Deficient Mice.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- MicroRNA Expression Profiles as Biomarkers of Response to Disease-Modifying Therapies in Multiple Sclerosis: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Dual-Targeting miR-219 and miR-146a in Multiple Sclerosis: Bridging Myelin Repair and Neuroinflammation for Novel Therapeutic Insights.Cellular and molecular neurobiology · 2026Review
- From Molecules to Models: miRNAs and Advanced Human Platforms of Neurodegeneration and Repair in Multiple Sclerosis.International journal of molecular sciences · 2025Review
- miR-146a Regulates Neuroinflammation and Immune Cell Function in Neurodegenerative Diseases.Current medical science · 2025Review
- Exosomal microRNAs as Early Transition Biomarkers from Recurrent-Remissive to Secondary Progressive Multiple Sclerosis.International journal of molecular sciences · 2025Review
- Identification of diagnostic microRNAs and their target genes in multiple sclerosis based on interactome networks using an in silico approach.Current journal of neurology · 2025Article
- White Matter Injury in Central Nervous System Disorders.Neuropsychiatric disease and treatment · 2025Review
- Neural regulation of the thymus: past, current, and future perspectives.Frontiers in immunology · 2025Review
- Review
- MicroRNAs dysregulated in multiple sclerosis affect the differentiation of CG-4 cells, an oligodendrocyte progenitor cell line.Frontiers in cellular neuroscience · 2024Article
- Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022Review
- The Role of Non-Coding RNAs in the Pathogenesis of Parkinson's Disease: Recent Advancement.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Histological and Top-Down Proteomic Analyses of the Visual Pathway in the Cuprizone Demyelination Model.Journal of molecular neuroscience : MN · 2022Article
- The Transcription Factor TFCP2L1 is Associated with Myelination via miR708-5p Regulation in the Peripheral Nerve System.Neurochemical research · 2022Article
- Proteomics of Multiple Sclerosis: Inherent Issues in Defining the Pathoetiology and Identifying (Early) Biomarkers.International journal of molecular sciences · 2021Review
- MicroRNAs in Prion Diseases-From Molecular Mechanisms to Insights in Translational Medicine.Cells · 2021Review
- Cladribine modifies functional properties of microglia.Clinical and experimental immunology · 2020Article
- Review
- Differential Expression of miRNAs and Behavioral Change in the Cuprizone-Induced Demyelination Mouse Model.International journal of molecular sciences · 2020Article
- Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The cuprizone (CPZ) model of multiple sclerosis (MS) was used to identify microRNAs (miRNAs) related to Methods: MicroRNAs were examined by Agilent Mouse miRNA Microarray in the corpus callosum during CPZ-induced demyelination and remyelination. Demyelination, axonal loss, changes in number of oligodendrocytes, OPCs, and macrophages/microglia was compared by histology/immunohistochemistry between KO and WT mice. Differential expression of target genes and proteins of miR-146a was analyzed in the transcriptome (4 × 44K Agilent Whole Mouse Genome Microarray) and proteome (liquid chromatography tandem mass spectrometry) of CPZ-induced de- and remyelination in WT mice. Levels of proinflammatory molecules in the corpus callosum were compared in WT versus KO mice by Meso Scale Discovery multiplex protein analysis. Results: miR-146a was increasingly upregulated during CPZ-induced de- and remyelination. The absence of miR-146a in KO mice protected against demyelination, axonal loss, body weight loss, and atrophy of thymus and spleen. The number of CNP Conclusion: During demyelination, absence of miR-146a reduced inflammatory responses, demyelination, axonal loss, the number of infiltrating macrophages, and increased the number of myelinating oligodendrocytes. The number of OPCs was slightly higher in the WT mice during remyelination, indicating a complex role of miR-146a during
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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.