Reprogramming macrophage orientation by microRNA 146b targeting transcription factor IRF5
Open accessAbstract
The regulation of macrophage orientation pathological conditions is important but still incompletely understood. Here, we show that IL-10 and Rag1 double knockout mice spontaneously develop colitis with dominant M1 macrophage phenotype, suggesting that IL-10 regulates macrophage orientation in inflammation. We demonstrate that IL-10 stimulation induced miR-146b expression, and that the expression of miR-146b was impaired in IL-10 deficient macrophages. Our data show that miR-146b targets IRF5, resulting in the regulation of macrophage activation. Furthermore, miR-146b deficient mice developed intestinal inflammation with enhanced M1 macrophage polarization. Finally, miR-146b mimic treatment significantly suppresses M1 macrophage activation and ameliorates colitis development in vivo. Collectively, the results suggest that IL-10 dependent miR-146b plays an important role in the modulation of M1 macrophage orientation.
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In a mouse model, knock-out of miR-146a led to colitis, which could be ameliorated upon administration of miR-146a mimic.
“In a mouse model, knock-out of miR-146a led to colitis, which could be ameliorated upon administration of miR-146a mimic [151].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [151]
The Results sections on miR-146b deficiency and mimic treatment report intestinal inflammation in miR-146b-knockout mice, but test the miR-146b mimic for colitis in IL-10-knockout mice. The paper identifies miR-146b, not miR-146a, throughout these findings; it does not report treating miR-146a-knockout mice with a miR-146a mimic. Page numbers were not available in our copy. (LLM, conf=0.88)
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Experimental — accuracy not yet measuredmiR-146b takes part in M2 polarization, is upregulated upon IL-10 stimulation, and targets interferon regulatory factor 5 (IRF5).
“The authors confirmed that miR-146b takes part in M2 polarization and it is upregulated upon IL-10 stimulation, and targets interferon regulatory factor 5 (IRF5).”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [151]
The Results section, “miR-146b Induced by IL-10 Suppresses M1 Macrophage Polarization” (page unavailable), and the Discussion support IL-10-dependent miR-146b expression and its targeting of IRF5. They describe suppression of M1 polarization, not a demonstrated role in M2 polarization. (LLM, conf=0.90)
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RETRACTED: Mir-124 Attenuates STAT3-Mediated TH17 Differentiation in Colitis-Driven Colon Cancer
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- Authors
- Peng, L., Zhang, H., Hao, Y., Xu, F., Yang, J., Zhang, R., Lu, G., Zheng, Z., Cui, M., Qi, C.-F., Chen, C., Wang, J., Hu, Y., Wang, D., Pierce, S., Li, L., & Xiong, H.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- National Institutes of Health (US)
- Virginia Tech (US)
- Jining Medical University (CN)
- Corresponding author
- Xiong, Huabao
- ORCID
- Venue
- EBioMedicine
- Publisher
- Elsevier BV
- Published
- 2016-12
- Volume
- 14
- Pages
- 83-96
- ISSN
- 2352-3964 (ISSN-L)
- PMC
- PMC5161420
- OpenAlex
- W2541610918
- Cited by
- 67
- References
- 48
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 7 · 2023: 5 · 2022: 8 · 2021: 7 · 2020: 9 · 2019: 8 · 2018: 9 · 2017: 4
- FWCI
- 4.25
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- EBioMedicine (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- VTechWorks (Virginia Tech) (submittedVersion, cc-by-nc-nd)
- Funders
- NIH (RO1AI104688)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Keywords
- macrophage polarization, M1 macrophage activation, microRNA-146b, IRF5, IL-10, RAG1, intestinal inflammation, colitis, microRNA target regulation
- MeSH terms
- Animals, Gene Expression Regulation, Macrophage Activation, Macrophages, T-Lymphocyte Subsets, Cytokines, Mice, Knockout, RNA Interference, MicroRNAs, Interferon Regulatory Factors, Mice, Cellular Reprogramming
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