miR-146a is a significant brake on autoimmunity, myeloproliferation, and cancer in mice
Open accessAbstract
Excessive or inappropriate activation of the immune system can be deleterious to the organism, warranting multiple molecular mechanisms to control and properly terminate immune responses. MicroRNAs (miRNAs), ∼22-nt-long noncoding RNAs, have recently emerged as key posttranscriptional regulators, controlling diverse biological processes, including responses to non-self. In this study, we examine the biological role of miR-146a using genetically engineered mice and show that targeted deletion of this gene, whose expression is strongly up-regulated after immune cell maturation and/or activation, results in several immune defects. Collectively, our findings suggest that miR-146a plays a key role as a molecular brake on inflammation, myeloid cell proliferation, and oncogenic transformation.
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miR-146a knockout mice develop LPS hypersensitivity, autoimmune disorders, myeloproliferative disorders, and lymphomas due to NF-κB dysregulation.
“Mice with miR-146a knock-out develop LPS hypersensitivity, autoimmune disorders, myeloproliferative disorders, and lymphomas [219] due to NF-κB dysregulation [220].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [219]
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“We identified three miRNA genes (miR-146a, miR-132, and miR-155) whose expression is sharply upregulated in response to LPS, and this list was later expanded further to include miR-9, miR-21, and miR-147 through the work of others (Bazzoni et al., 2009; Liu et al., 2009; Sheedy et al., 2010).”
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- Authors
- Boldin, M. P., Taganov, K. D., Rao, D. S., Yang, L., Zhao, J. L., Kalwani, M., Garcia-Flores, Y., Luong, M., Devrekanli, A., Xu, J., Sun, G., Tay, J., Linsley, P. S., & Baltimore, D.
- Affiliations
- Regulus Therapeutics (United States) (US)
- California Institute of Technology (US)
- Corresponding author
- Boldin, Mark P.
- Baltimore, David
- ORCID
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2011-05-09
- Volume
- 208
- Issue
- 6
- Pages
- 1189-1201
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC3173243
- OpenAlex
- W2098199767
- Cited by
- 861
- References
- 7
- Citations by year
- 2026: 24 · 2025: 20 · 2024: 53 · 2023: 38 · 2022: 42 · 2021: 71 · 2020: 71 · 2019: 57 · 2018: 69 · 2017: 61 · 2016: 64 · 2015: 66 · 2014: 83 · 2013: 65 · 2012: 55
- FWCI
- 24.38
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion, cc-by-nc-sa)
- eScholarship (California Digital Library) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by-nc-sa)
- Funders
- California Institute of Technology
- National Institutes of Health
- National Cancer Institute (K08CA133521)
- National Institute of Allergy and Infectious Diseases (R01AI079243)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- miR-146a, microRNA, autoimmunity, myeloproliferation, inflammation, myeloid cell proliferation, oncogenic transformation, immune regulation, gene deletion, immune cell activation, post-transcriptional regulation
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Female, Humans, Inflammation, Lipopolysaccharides, Male, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, Neoplasms, RNA Processing, Post-Transcriptional, Autoimmunity, Up-Regulation, Mice, Knockout, 3' Untranslated Regions, MicroRNAs, TNF Receptor-Associated Factor 6, Cell Proliferation, Mice, Interleukin-1 Receptor-Associated Kinases
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