Interleukin-4 regulates macrophage polarization via the MAPK signaling pathway to protect against atherosclerosis
Open accessAbstract
Our study aimed to investigate the effects of interleukin-4 (IL-4) on macrophage polarization, as well as its role in the development of atherosclerosis. Human peripheral blood mononuclear cells (PBMCs) were isolated and randomly divided into 3 groups: control group, ox-LDL group, and ox-LDL + IL-4 groups. The expression of M1/M2 macrophage surface markers such as TNF-α, CD68, and CD206 were analyzed by western blot. Cell viability was determined using the MTT assay. Measurement of CD86/CD206 expression ratio (M1/M2 ratio) was performed via flow cytometry. In addition, ApoE(-/-) mice on a C57BL/6 background were subjected to high-fat diets, and were used as a model of atherosclerosis. Atherosclerotic lesion area was quantified after mice were treated with ox-LDL and IL-4. Finally, expression of phosphorylated MAPK signaling molecules such as p-ERK and p-JNK was quantified using western blot. The expression of TNF-α and CD86 markedly increased after cells were treated with ox-LDL, whereas the expression of CD206 markedly increased after PBMCs were treated with IL-4. It is possible that IL-4 could decrease ox-LDL-induced cell viability and the CD86/CD206 (M1/M2) ratio. Additionally, IL-4 intervention attenuated ox-LDL-induced atherosclerotic lesions in ApoE(-/-) mice, and decreased ox- LDL-induced expression of p-ERK and p-JNK. Our findings indicate that IL-4 may induce macrophages to take on an M2 phenotype in order to resolve inflammation via inhibition of MAPK signaling pathways, thereby protecting against atherosclerosis. IL-4 may serve as an intervention target for atherosclerosis.
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CD68 and CD86 are markers for M1 macrophages, and CD68 and CD206 are markers for M2 macrophages.
“Macrophage phenotypic markers, CD68 and CD86 for M1 and CD68 and CD206 for M2, were selected following the previous study [31,32].”
From Substrate stiffness modulates bone marrow-derived macrophage polarization through NF-κB signaling pathway (2020) · cites this paper as [32]
The Flow cytometry and Surface marker expression sections use CD86 to indicate M1 polarization and CD206 to indicate M2 polarization. The Western blot section measures CD68, but the paper does not identify CD68 as part of both the M1 and M2 marker pairs stated in the claim. Page numbers are unavailable in our copy. (LLM, conf=0.84)
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- Authors
- Zhao, X. N., Li, Y. N., & Wang, Y. T.
- Affiliations
- Chinese PLA General Hospital (CN)
- ORCID
- Wang, Y.T.
- Venue
- Genetics and Molecular Research
- Publisher
- Genetics and Molecular Research
- Published
- 2016
- Volume
- 15
- Issue
- 1
- ISSN
- 1676-5680 (ISSN-L)
- OpenAlex
- W2339577610
- Cited by
- 44
- References
- 31
- Citations by year
- 2025: 4 · 2024: 1 · 2023: 6 · 2022: 2 · 2021: 1 · 2020: 6 · 2019: 7 · 2018: 9 · 2017: 8
- FWCI
- 4.84
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genetics and Molecular Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- IL-4, macrophage polarization, atherosclerosis, MAPK signaling, M2 macrophage phenotype, M1/M2 ratio, oxidized LDL, ERK1/2 phosphorylation, JNK phosphorylation, ApoE-deficient mice, high-fat diet, inflammation resolution
- MeSH terms
- Animals, Apolipoproteins E, Cells, Cultured, Lipoproteins, LDL, Macrophages, Mice, Inbred C57BL, Phosphorylation, Signal Transduction, Interleukin-4, Atherosclerosis, Mice
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