PPAR agonist-induced reduction of Mcp1 in atherosclerotic plaques of obese, insulin-resistant mice depends on adiponectin-induced Irak3 expression
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Synthetic peroxisome proliferator-activated receptor (PPAR) agonists are used to treat dyslipidemia and insulin resistance. In this study, we examined molecular mechanisms that explain differential effects of a PPARα agonist (fenofibrate) and a PPARγ agonist (rosiglitazone) on macrophages during obesity-induced atherogenesis. Twelve-week-old mice with combined leptin and LDL-receptor deficiency (DKO) were treated with fenofibrate, rosiglitazone or placebo for 12 weeks. Only rosiglitazone improved adipocyte function, restored insulin sensitivity, and inhibited atherosclerosis by decreasing lipid-loaded macrophages. In addition, it increased interleukin-1 receptor-associated kinase-3 (Irak3) and decreased monocyte chemoattractant protein-1 (Mcp1) expressions, indicative of a switch from M1 to M2 macrophages. The differences between fenofibrate and rosiglitazone were independent of Pparγ expression. In bone marrow-derived macrophages (BMDM), we identified the rosiglitazone-associated increase in adiponectin as cause of the increase in Irak3. Interestingly, the deletion of Irak3 in BMDM (IRAK3(-/-) BMDM) resulted in activation of the canonical NFκB signaling pathway and increased Mcp1 protein secretion. Rosiglitazone could not decrease the elevated Mcp1 secretion in IRAK3(-/-) BMDM directly and fenofibrate even increased the secretion, possibly due to increased mitochondrial reactive oxygen species production. Furthermore, aortic extracts of high-fat insulin-resistant LDL-receptor deficient mice, with lower adiponectin and Irak3 and higher Mcp1, showed accelerated atherosclerosis. In aggregate, our results emphasize an interaction between PPAR agonist-mediated increase in adiponectin and macrophage-associated Irak3 in the protection against atherosclerosis by PPAR agonists.
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PPARα is a therapeutic target for lipid metabolism dysfunction.
“Peroxisome proliferator-activated receptor alpha (PPARα), a therapeutic target for lipid metabolism dysfunction [32]”
From Fibrates as drugs with senolytic and autophagic activity for osteoarthritis therapy (2019) · cites this paper as [32]
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Miao, Y., Mei, Q., Fu, C., Liao, M., Liu, Y., Xu, X., Li, X., Zhao, S., & Xiang, T. (2021) · Figshare · doi:10.6084/m9.figshare.14471507
Miao, Y., Mei, Q., Fu, C., Liao, M., Liu, Y., Xu, X., Li, X., Zhao, S., & Xiang, T. (2021) · Figshare · doi:10.6084/m9.figshare.14471510
Miao, Y., Mei, Q., Fu, C., Liao, M., Liu, Y., Xu, X., Li, X., Zhao, S., & Xiang, T. (2021) · Figshare · doi:10.6084/m9.figshare.14471516
Miao, Y., Mei, Q., Fu, C., Liao, M., Liu, Y., Xu, X., Li, X., Zhao, S., & Xiang, T. (2021) · Figshare · doi:10.6084/m9.figshare.14471513
Vastrad, B. M., & Vastrad, C. M. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.08.15.608116
Vastrad, B. M., & Vastrad, C. M. (2024) · Egyptian Journal of Medical Human Genetics · doi:10.1186/s43042-024-00584-5
- Authors
- Hulsmans, M., Geeraert, B., Arnould, T., Tsatsanis, C., & Holvoet, P.
- Affiliations
- KU Leuven (BE)
- University of Namur (BE)
- University of Crete (GR)
- Corresponding author
- Holvoet, Paul
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-04-19
- Volume
- 8
- Issue
- 4
- Pages
- e62253
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3631170
- OpenAlex
- W1990837317
- Cited by
- 39
- References
- 47
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 5 · 2023: 2 · 2022: 3 · 2021: 3 · 2020: 1 · 2019: 4 · 2018: 2 · 2017: 4 · 2016: 5 · 2015: 4 · 2014: 4
- FWCI
- 1.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Repository of the University of Namur (publishedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Vlaamse regering
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- PPAR agonists, rosiglitazone, fenofibrate, adiponectin, IRAK3, MCP-1, atherosclerosis, macrophage polarization, M1/M2 macrophages, obesity, insulin resistance, NF-κB signaling, mitochondrial reactive oxygen species, LDL receptor-deficient mice, leptin deficiency, bone marrow-derived macrophages
- MeSH terms
- Rosiglitazone, Animals, Inflammation, Insulin, Insulin Resistance, Macrophages, Mice, Inbred C57BL, Obesity, Fenofibrate, Adipocytes, Chemokine CCL2, Leptin, Thiazolidinediones, Peroxisome Proliferator-Activated Receptors, PPAR alpha, PPAR gamma, Mice, Adiponectin, Interleukin-1 Receptor-Associated Kinases, Plaque, Atherosclerotic, Diet, High-Fat
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