Regulation of miR-146a by RelA/NFkB and p53 in STHdhQ111/HdhQ111 Cells, a Cell Model of Huntington's Disease

Ghose, Jayeeta; Sinha, Mithun; Das, Eashita; Jana, Nihar R.; Bhattacharyya, Nitai P.

doi:10.1371/journal.pone.0023837

Cited by 98Genetic Neurodegenerative DiseasesMicroRNA in disease regulationNeuroinflammation and Neurodegeneration Mechanisms

Regulation of miR-146a by RelA/NFkB and p53 in STHdhQ111/HdhQ111 Cells, a Cell Model of Huntington's Disease

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Ghose, Jayeeta, Sinha, Mithun, Das, Eashita, Jana, Nihar R., Bhattacharyya, Nitai P.·2011·PLoS ONE

DOI 10.1371/journal.pone.0023837PMC PMC3162608

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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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Other tumor suppressors among them Fbw7 and p53 have also been reported to target NF-κB.
“It is noteworthy that other tumor suppressors among them Fbw7 (43) and p53 have also been reported to target NF-κB (44).”
From Tumor suppressor PDCD4 inhibits NF-κB-dependent transcription in human glioblastoma cells by direct interaction with p65 (2014) · cites this paper as [44]

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Altered microRNAs in STHdhQ111/HdhQ111 cells: miR-146a targets TBP
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Regulation of MicroRNAs by p53 and NFkB in cell models of Huntington s disease
Ghose, J. (2014) · Shodhganga
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MicroRNAs Located in the Hox Gene Clusters Are Implicated in Huntington's Disease Pathogenesis
Hoss, A. G., Kartha, V. K., Dong, X., Latourelle, J. C., Dumitriu, A., Hadzi, T. C., MacDonald, M. E., Gusella, J. F., Akbarian, S., Chen, J., et al. (2014) · PLoS Genetics · doi:10.1371/journal.pgen.1004188 · Cited by 128 · see citing works

Authors: Ghose, J., Sinha, M., Das, E., Jana, N. R., & Bhattacharyya, N. P.
Affiliations: Saha Institute of Nuclear Physics (IN)
National Brain Research Centre (IN)
Corresponding author: Bhattacharyya, Nitai P.
ORCID: Ghose, Jayeeta
Sinha, Mithun
Jana, Nihar R.
Bhattacharyya, Nitai P.
Venue: PLoS ONE
Publisher: Public Library of Science (PLoS)
Published: 2011-08-26
Volume: 6
Issue: 8
Pages: e23837
ISSN: 1932-6203 (ISSN-L)
DOI: 10.1371/journal.pone.0023837
PMC: PMC3162608
OpenAlex: W2011695980
Cited by: 98
References: 72
Citations by year: 2026: 2 · 2025: 2 · 2024: 4 · 2023: 8 · 2022: 4 · 2021: 7 · 2020: 8 · 2019: 3 · 2018: 6 · 2017: 7 · 2016: 8 · 2015: 8 · 2014: 10 · 2013: 11 · 2012: 9
FWCI: 4.11
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (unspecified)
Locations: PLoS ONE (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Figshare (submittedVersion, cc-by)
Funders: Massachusetts General Hospital
Department of Atomic Energy, Government of India
Nuclear Physics
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: Huntington's disease, miR-146a, p53, microRNA regulation, miR-125b, miR-150, mutant huntingtin, R6/2 mice, HSP70, transcriptional regulation, striatum, polyglutamine
MeSH terms: Huntingtin Protein, Gene Expression Regulation, Humans, Huntington Disease, Nerve Tissue Proteins, Nuclear Proteins, Tumor Cells, Cultured, Tumor Suppressor Protein p53, NF-kappa B, MicroRNAs, Transcription Factor RelA

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Regulation of miR-146a by RelA/NFkB and p53 in STHdhQ111/HdhQ111 Cells, a Cell Model of Huntington's Disease

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