ArticlePloS one2011
Regulation of miR-146a by RelA/NFkB and p53 in STHdh(Q111)/Hdh(Q111) cells, a cell model of Huntington's disease.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 98 citations in OpenAlex.
- miR-146a Regulates Neuroinflammation and Immune Cell Function in Neurodegenerative Diseases.Current medical science · 2025Review
- Proteomimetic polymer blocks mitochondrial damage, rescues Huntington's neurons, and slows onset of neuropathology in vivo.Science advances · 2024Article
- IL-33 Induces Cellular and Exosomal miR-146a Expression as a Feedback Inhibitor of Mast Cell Function.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Non-coding RNAs in human health and disease: potential function as biomarkers and therapeutic targets.Functional & integrative genomics · 2023Review
- The transcription factor TBP promotes hepatocellular carcinoma progression by activating AKT3.American journal of cancer research · 2023Article
- microRNA 146a ameliorates retinal damage in experimental autoimmune uveitis.Frontiers in ophthalmology · 2023Article
- A Comprehensive Bioinformatics Approach to Identify Molecular Signatures and Key Pathways for the Huntington Disease.Bioinformatics and biology insights · 2023Article
- A Review of Molecular Interplay between Neurotrophins and miRNAs in Neuropsychological Disorders.Molecular neurobiology · 2022Review
- Precision machine learning to understand micro-RNA regulation in neurodegenerative diseases.Frontiers in molecular neuroscience · 2022Review
- An Emerging Role of miRNAs in Neurodegenerative Diseases: Mechanisms and Perspectives onAntioxidants & redox signaling · 2021Review
- Huntington's Chorea-a Rare Neurodegenerative Autosomal Dominant Disease: Insight into Molecular Genetics, Prognosis and Diagnosis.Applied biochemistry and biotechnology · 2021Review
- Fibroblast Growth Factor 9 Stimulates Neuronal Length Through NF-kB Signaling in Striatal Cell Huntington's Disease Models.Molecular neurobiology · 2021Article
- MicroRNAs in Huntington's Disease: Diagnostic Biomarkers or Therapeutic Agents?Frontiers in cellular neuroscience · 2021Review
- Review
- Effects of Mycoplasmas on the Host Cell Signaling Pathways.Pathogens (Basel, Switzerland) · 2020Review
- Functional roles and networks of non-coding RNAs in the pathogenesis of neurodegenerative diseases.Journal of biomedical science · 2020Review
- Epigenetic mechanisms of neurodegenerative diseases and acute brain injury.Neurochemistry international · 2020Review
- PD173074 blocks G1/S transition via CUL3-mediated ubiquitin protease in HepG2 and Hep3B cells.PloS one · 2020Article
- MiR-146a down-regulates inflammatory response by targeting TLR3 and TRAF6 in Coxsackievirus B infection.RNA (New York, N.Y.) · 2020Article
- Role of Nuclear Factor Kappa B (NF-κB) Signalling in Neurodegenerative Diseases: An Mechanistic Approach.Current neuropharmacology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is caused by the expansion of N-terminal polymorphic poly Q stretch of the protein huntingtin (HTT). Deregulated microRNAs and loss of function of transcription factors recruited to mutant HTT aggregates could cause characteristic transcriptional deregulation associated with HD. We observed earlier that expressions of miR-125b, miR-146a and miR-150 are decreased in STHdh(Q111)/Hdh(Q111) cells, a model for HD in comparison to those of wild type STHdh(Q7)/Hdh(Q7) cells. In the present manuscript, we show by luciferase reporter assays and real time PCR that decreased miR-146a expression in STHdh(Q111)/Hdh(Q111) cells is due to decreased expression and activity of p65 subunit of NFkB (RelA/NFkB). By reporter luciferase assay, RT-PCR and western blot analysis, we also show that both miR-150 and miR-125b target p53. This partially explains the up regulation of p53 observed in HD. Elevated p53 interacts with RelA/NFkB, reduces its expression and activity and decreases the expression of miR-146a, while knocking down p53 increases RelA/NFkB and miR-146a expressions. We also demonstrate that expression of p53 is increased and levels of RelA/NFkB, miR-146a, miR-150 and miR-125b are decreased in striatum of R6/2 mice, a mouse model of HD and in cell models of HD. In a cell model, this effect could be reversed by exogenous expression of chaperone like proteins HYPK and Hsp70. We conclude that (i) miR-125b and miR-150 target p53, which in turn regulates RelA/NFkB and miR-146a expressions; (ii) reduced miR-125b and miR-150 expressions, increased p53 level and decreased RelA/NFkB and miR-146a expressions originate from mutant HTT (iii) p53 directly or indirectly regulates the expression of miR-146a. Our observation of interplay between transcription factors and miRNAs using HD cell model provides an important platform upon which further work is to be done to establish if such regulation plays any role in HD pathogenesis.
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