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MicroRNA let-7c Regulates Macrophage Polarization
Open accessAbstract
Macrophages demonstrate a high level of plasticity, with the ability to undergo dynamic transition between M1 and M2 polarized phenotypes. The role of microRNAs (miRNAs) in regulating macrophage polarization has been largely undefined. In this study, we found that miRNA let-7c is expressed at a higher level in M-BMM (M2 macrophages) than in GM-BMM (M1 macrophages). let-7c levels are also greater in alveolar macrophages from fibrotic lungs as compared with those from normal lungs. let-7c expression was decreased when M-BMM converted to GM-BMM, whereas it increased when GM-BMM converted to M-BMM. LPS stimulation reduced let-7c expression in M-BMM. We found that overexpression of let-7c in GM-BMM diminished M1 phenotype expression while promoting polarization to the M2 phenotype. In contrast, knockdown of let-7c in M-BMM promoted M1 polarization and diminished M2 phenotype expression. We found that let-7c targets C/EBP-δ, a transcriptional factor that plays an important role in inflammatory response. Furthermore, we found that let-7c regulates bactericidal and phagocytic activities of macrophages, two functional phenotypes implicated in macrophage polarization. Our data suggest that the miRNA let-7c plays an important role in regulating macrophage polarization.
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“Expression of let-7c is suppressed by LPS, whereas its upregulation results in a change from the M1 to M2 phenotype by targeting the C/EBP-δ transcription factor [110].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [110]
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“Overexpression of let-7c, by promoting the M2 phenotype, increases phagocytosis of apoptotic cells, whereas its knockdown decreases it [110].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [110]
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González, C., Cimini, M., Mallaredy, V., Benedict, C., Joladarashi, D., Thej, C., Cheng, Z. A., Trungcao, M., Rai, A. K., Garikipati, V. N. S., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.02.21.639391
Metadata
- Authors
- Banerjee, S., Xie, N., Cui, H., Tan, Z., Yang, S., Icyuz, M., Abraham, E., & Liu, G.
- Affiliations
- University of Alabama at Birmingham (US)
- Wake Forest University Health Sciences (US)
- Corresponding author
- Banerjee, Sami
- Xie, Na
- Cui, Huachun
- Tan, Zheng
- Yang, Shanzhong
- Icyuz, Mert
- Liu, Gang
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-06
- Volume
- 190
- Issue
- 12
- Pages
- 6542-6549
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3679284
- OpenAlex
- W1927296860
- Cited by
- 320
- References
- 62
- Citations by year
- 2026: 5 · 2025: 18 · 2024: 24 · 2023: 20 · 2022: 28 · 2021: 33 · 2020: 26 · 2019: 26 · 2018: 31 · 2017: 22 · 2016: 21 · 2015: 29 · 2014: 17 · 2013: 7
- FWCI
- 13.65
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL 076206, R21HL097218, HL-105473, R01HL105473, R01HL076206, HL-097218)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (P30AR048311)
- 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 › Immunology and Microbiology › Immunology › Macrophage Migration Inhibitory Factor
- Keywords
- let-7c microRNA, macrophage polarization, M1/M2 macrophages, C/EBPδ, alveolar macrophages, pulmonary fibrosis, lipopolysaccharide, phagocytosis, bactericidal activity, bone marrow-derived macrophages
- MeSH terms
- Animals, Cell Differentiation, Flow Cytometry, Macrophages, Mice, Inbred BALB C, Mice, Inbred C57BL, Phenotype, Transfection, Blotting, Western, Cell Polarity, Reverse Transcriptase Polymerase Chain Reaction, MicroRNAs, Mice, Real-Time Polymerase Chain Reaction
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