Lack of Interleukin-1β Decreases the Severity of Atherosclerosis in ApoE-Deficient Mice
Open accessAbstract
OBJECTIVE: Atherosclerosis is considered to be a chronic inflammatory disease and many cytokines participate in the development of atherosclerosis. We focused on the role of interleukin-1beta (IL-1beta), one of the proinflammatory cytokines secreted by monocytes/macrophages, in the progression of atherosclerosis. METHODS AND RESULTS: We generated mice lacking both apoE and IL-1beta. The sizes of atherosclerotic lesions at the aortic sinus in apoE-/-/IL-1beta-/-mice at 12 and 24 weeks of age showed a significant decrease of approximately 30% compared with apoE-/-/IL-1beta+/+ mice, and the percentage of the atherosclerotic area to total area of apoE-/-/IL-1beta-/- at 24 weeks of age also showed a significant decrease of about 30% compared with apoE-/-/IL-1beta+/+. The mRNA levels of vascular cell adhesion molecule (VCAM)-1 and monocyte chemotactic protein-1 in the apoE-/-/IL-1beta-/- aorta were significantly reduced compared with the apoE-/-/IL-1beta+/+. Furthermore, VCAM-1 was also reduced at the protein level in apoE-/-/IL-1beta-/- aorta compared with apoE-/-/IL-1beta+/+. CONCLUSIONS: The lack of IL-1beta decreases the severity of atherosclerosis in apoE deficient mice, possibly through increased expressions of VCAM-1 and monocyte chemotactic protein-1 in the aorta.
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Vascular inflammation stimulates the production of chemoattractants and molecules such as monocyte chemotactic proteins and vascular cell adhesion molecule 1 in endothelium.
“Vascular inflammation stimulates the production of chemoattractants and molecules such as monocyte chemotactic proteins and vascular cell adhesion molecule 1 in endothelium [242,243,244].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [244]
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- Authors
- Kirii, H., Niwa, T., Yamada, Y., Wada, H., Saito, K., Iwakura, Y., Asano, M., Moriwaki, H., & Seishima, M.
- Affiliations
- Kanazawa University (JP)
- Venue
- Arteriosclerosis Thrombosis and Vascular Biology
- Published
- 2003-04
- Volume
- 23
- Issue
- 4
- Pages
- 656-660
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2100748836
- Cited by
- 748
- References
- 28
- Citations by year
- 2026: 11 · 2025: 32 · 2024: 29 · 2023: 46 · 2022: 42 · 2021: 49 · 2020: 51 · 2019: 40 · 2018: 47 · 2017: 40 · 2016: 30 · 2015: 42 · 2014: 38 · 2013: 41 · 2012: 32
- FWCI
- 7.03
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- public-domain
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion, public-domain)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (13470517)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- IL-1β, atherosclerosis, apolipoprotein E deficiency, inflammatory cytokines, VCAM-1, MCP-1, atherosclerotic plaque severity, atherosclerosis progression
- MeSH terms
- Animals, Aorta, Aortic Valve Stenosis, Apolipoproteins E, Arteriosclerosis, Cell Movement, Gene Expression Regulation, Interleukin-1, Lipids, Macrophages, Male, Mice, Inbred C57BL, Monocytes, RNA, Messenger, Tunica Intima, Mice, Knockout, Chemokine CCL2, Vascular Cell Adhesion Molecule-1, Mice
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