miR-24 Regulates Macrophage Polarization and Plasticity
Open accessAbstract
OBJECTIVE: (Pg), and revealed cigarette smoke extract as an environmental modifier of Pg LPS structure (Pg CSE) impacting macrophage miRNA responses. This study was designed to investigate the role of miR-24 on macrophage polarization and plasticity. METHODS: monocytes isolated from peripheral blood mononuclear cells (PBMCs) by MACS positive selection and transfected with miR-24 miRNA mimics, inhibitors, or negative control mimic; followed by stimulation with cytokines and/or LPS under various conditions representing key stages of macrophage activation. Macrophage activation and polarization was assessed using assays for cytokine production (ELISA) and protein expression (flow cytometry, immunoblot). MiR-24 expression was assessed by RT-PCR. RESULTS: Stimulation of macrophages with LPSs of Aa, Pg, and Pg CSE origin resulted in dissimilar levels of cytokine expression and differential expression of miR-24. Overexpression of miR-24 inhibited cytokine secretion in response to LPS. Priming of macrophages with interferon gamma (IFN-γ) did not overcome this inhibitory effect, but classical activation of macrophages with IFN-γ plus TNF-α, TNF-β, or IL-17, modulated the pattern of miR-24 mediated suppression in a cytokine-specific fashion. Overexpression of miR-24 enhanced CD206 upregulation during alternative macrophage activation and inhibited its downregulation in macrophage transitioning from alternative to classical activation states. Overexpression of miR-24 resulted in reduced expression of the Class 1A PI 3-kinase subunit p110 delta (p110δ). CONCLUSION: Pathogen- and environment-specific modifications in LPS alter the expression of cytokines and miR-24 in human macrophages. MiR-24 is a negative regulator of macrophage classical activation by LPS and promotes alternative activation under conditions of polarization and plasticity. MiR-24 mediated inhibition of LPS-induced cytokine secretion is dependent upon macrophage activation state at the point of stimulation, and this may be due to the degree to which p110δ is involved in the intracellular signaling pathway/s that transduce receptor ligation into cytokine induction. While important differences were observed in the effect of miR-24 on macrophages, these data indicate that overexpression of miR-24 would be predominantly anti-inflammatory.
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miR-24 is a negative regulator of macrophage classical activation induced by LPS; its mechanism involves modulation of phosphoinositide 3-kinase (PI3K) and further inhibition of cytokine synthesis.
“MiR-24 is an example of a negative regulator of macrophage classical activation induced by LPS. The identified mechanism of action involves modulation of phosphoinositide 3-kinase (PI3K) and further inhibition of cytokine synthesis [124].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [124]
The Introduction and Abstract Conclusion identify miR-24 as a negative regulator of LPS-induced classical macrophage activation, and the Abstract Results report inhibited cytokine secretion and reduced expression of the PI3K subunit p110δ. But the Abstract Conclusion says p110δ involvement in cytokine inhibition “may” explain the effect; the Discussion also presents it as a possibility, not an identified mechanism. (LLM, conf=0.88)
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- Authors
- Afsar R. Naqvi, J. B. F., & Nares, S.
- Affiliations
- University of Illinois Chicago (US)
- Corresponding author
- Nares, Salvador
- ORCID
- Nares, Salvador
- Venue
- Journal of Clinical & Cellular Immunology
- Publisher
- OMICS Publishing Group
- Published
- 2015
- Volume
- 06
- Issue
- 05
- ISSN
- 2155-9899 (ISSN-L)
- PMC
- PMC4721581
- OpenAlex
- W2416233116
- Cited by
- 65
- References
- 33
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 7 · 2023: 1 · 2022: 12 · 2021: 10 · 2020: 5 · 2019: 3 · 2018: 8 · 2017: 11 · 2016: 3
- FWCI
- 3.62
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by
- Locations
- Journal of Clinical & Cellular Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion, cc-by)
- Funders
- University of South Carolina
- National Institute of Dental and Craniofacial Research (R01DE021052)
- 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 › Immune Response and Inflammation
- Keywords
- miR-24, macrophage polarization, macrophage plasticity, cigarette smoke extract, lipopolysaccharide, macrophage activation, alternative activation, classical activation, CD206, p110δ, PI3K signaling, cytokine production, interferon-gamma, anti-inflammatory microRNA, lung inflammation, environmental modifiers
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