ArticleMultiple sclerosis (Houndmills, Basingstoke, England)2018
Hypermethylation of MIR21 in CD4+ T cells from patients with relapsing-remitting multiple sclerosis associates with lower miRNA-21 levels and concomitant up-regulation of its target genes.
Article in Multiple sclerosis (Houndmills, Basingstoke, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- The role of microRNAs and long non-coding RNAs in epigenetic regulation of T cells: implications for autoimmunity.Frontiers in immunology · 2025Pooled it
- Evaluating miRNA Sequencing and Integrative Proteomics for Identifying Plasma miRNAs as Potential Pharmacodynamic Biomarkers of IFNβ-1a Biologics.Clinical and translational science · 2025Trial
- Critical roles of miR-21 in promotions angiogenesis: friend or foe?Clinical and experimental medicine · 2025Review
- miRNA-21, an Important Regulator of Autoimmune Diseases.Current molecular medicine · 2025Review
- Exploring regulatory mechanisms on miRNAs and their implications in inflammation-related diseases.Clinical and experimental medicine · 2024Review
- Evaluation of Cell-Specific Epigenetic Age Acceleration in People With Multiple Sclerosis.Neurology · 2023Article
- Whole-blood methylation signatures are associated with and accurately classify multiple sclerosis disease severity.Clinical epigenetics · 2022Article
- Quantitative proteomics reveals protein dysregulation during T cell activation in multiple sclerosis patients compared to healthy controls.Clinical proteomics · 2022Article
- Construction of miRNA-regulated drug-pathway network to screen drug repurposing candidates for multiple sclerosis.Medicine · 2022Article
- MicroRNA-21 Is a Versatile Regulator and Potential Treatment Target in Central Nervous System Disorders.Frontiers in molecular neuroscience · 2022Review
- MicroRNAs as T Lymphocyte Regulators in Multiple Sclerosis.Frontiers in molecular neuroscience · 2022Review
- Sex, aging and immunity in multiple sclerosis and experimental autoimmune encephalomyelitis: An intriguing interaction.Frontiers in neurology · 2022Review
- Contribution of Dysregulated DNA Methylation to Autoimmunity.International journal of molecular sciences · 2021Review
- MicroRNAs, Multiple Sclerosis, and Depression.International journal of molecular sciences · 2021Review
- Imprinted Genes and Multiple Sclerosis: What Do We Know?International journal of molecular sciences · 2021Review
- hPMSCs-Derived Exosomal miRNA-21 Protects Against Aging-Related Oxidative Damage of CD4Frontiers in immunology · 2021Article
- Epigenetic differences at the HTR2A locus in progressive multiple sclerosis patients.Scientific reports · 2020Article
- Modulators of MicroRNA Function in the Immune System.International journal of molecular sciences · 2020Review
- Aberrant DNA methylation profile exacerbates inflammation and neurodegeneration in multiple sclerosis patients.Journal of neuroinflammation · 2020Review
- Mechanisms of M2 Macrophage-Derived Exosomal Long Non-coding RNA PVT1 in Regulating Th17 Cell Response in Experimental Autoimmune Encephalomyelitisa.Frontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 6 countries.
Funding
Abstract
backgroundMultiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system caused by genetic and environmental factors. DNA methylation, an epigenetic mechanism that controls genome activity, may provide a link between genetic and environmental risk factors.
objectiveWe sought to identify DNA methylation changes in CD4+ T cells in patients with relapsing-remitting (RR-MS) and secondary-progressive (SP-MS) disease and healthy controls (HC).
methodsWe performed DNA methylation analysis in CD4+ T cells from RR-MS, SP-MS, and HC and associated identified changes with the nearby risk allele, smoking, age, and gene expression.
resultsWe observed significant methylation differences in the VMP1/MIR21 locus, with RR-MS displaying higher methylation compared to SP-MS and HC. VMP1/MIR21 methylation did not correlate with a known MS risk variant in VMP1 or smoking but displayed a significant negative correlation with age and the levels of mature miR-21 in CD4+ T cells. Accordingly, RR-MS displayed lower levels of miR-21 compared to SP-MS, which might reflect differences in age between the groups, and healthy individuals and a significant enrichment of up-regulated miR-21 target genes.
conclusionDisease-related changes in epigenetic marking of MIR21 in RR-MS lead to differences in miR-21 expression with a consequence on miR-21 target genes.
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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.