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miR-125a-5p Regulates Differential Activation of Macrophages and Inflammation
Open accessAbstract
Macrophage activation is a central event in immune responses. Macrophages undergoing classical activation (M1 macrophages) are proinflammatory, whereas alternatively activated macrophages (M2 macrophages) are generally anti-inflammatory. miRNAs play important regulatory roles in inflammatory response. However, the manner in which miRNAs regulate macrophage activation in response to different environmental cues has not been well defined. In this study, we found that M-BMM macrophages (M2) express greater levels of miR-125a-5p than do GM-BMM macrophages (M1). Stimulation of macrophages through TLR2 and TLR4 but not through TLR3 enhanced miR-125a-5p expression. Up-regulation of miR-125a-5p after TLR2/4 activation requires the adaptor MYD88 but not TRIF. Overexpression of miR-125a-5p diminished M1 phenotype expression induced by LPS but promoted M2 marker expression induced by IL-4. In contrast, knockdown of miR-125a-5p promoted M1 polarization and diminished IL-4-induced M2 marker expression. We found that miR-125a-5p targets KLF13, a transcriptional factor that has an important role in T lymphocyte activation and inflammation. KLF13 knockdown had similar effects on M1 activation as did miR-125a-5p overexpression. In addition, miR-125a-5p regulates phagocytic and bactericidal activities of macrophages. Our data suggest that miR-125a-5p has an important role in suppressing classical activation of macrophages while promoting alternative activation.
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“M1 macrophages, when transfected with miR-125a-5p, are less potent in exerting bactericidal activity against Escherichia coli, which results from targeting Kruppel-like Factor 13 (KLF13) and promotion of M2 polarization [138].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [138]
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“Stimulation of TLR2 and TLR4 leads to upregulation of miR-125a-5p in an MYD88-dependent manner and subsequently promotes the M2 phenotype [138]”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [138]
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Metadata
- Authors
- Banerjee, S., Cui, H., Xie, N., Tan, Z., Yang, S., Icyuz, M., Thannickal, V. J., Abraham, E., & Liu, G.
- Affiliations
- University of Alabama at Birmingham (US)
- Wake Forest University Health Sciences (US)
- Corresponding author
- Liu, Gang
- ORCID
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 288
- Issue
- 49
- Pages
- 35428-35436
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC3853290
- OpenAlex
- W1989029018
- Cited by
- 258
- References
- 52
- Citations by year
- 2026: 10 · 2025: 12 · 2024: 19 · 2023: 25 · 2022: 29 · 2021: 33 · 2020: 17 · 2019: 25 · 2018: 24 · 2017: 19 · 2016: 21 · 2015: 14 · 2014: 9
- FWCI
- 5.16
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL 076206, HL114470, HL-105473, R01HL105473, R01HL076206, P01HL114470)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (P30AR048311)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- miR-125a-5p, macrophage polarization, M1 macrophages, M2 macrophages, classical activation, alternative activation, KLF13, TLR2, TLR4, MyD88, TRIF, LPS, IL-4, inflammation, phagocytosis, bactericidal activity, bone marrow-derived macrophages
- MeSH terms
- Animals, Escherichia coli, Inflammation, Macrophage Activation, Macrophages, Mice, Inbred C57BL, Repressor Proteins, Up-Regulation, Mice, Knockout, Cell Cycle Proteins, Adaptor Proteins, Vesicular Transport, MicroRNAs, Toll-Like Receptor 2, Toll-Like Receptor 4, Mice, Kruppel-Like Transcription Factors, Myeloid Differentiation Factor 88, Gene Knockdown Techniques
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