Cited by 748Atherosclerosis and Cardiovascular DiseasesCholesterol and Lipid MetabolismInflammasome and immune disorders

Lack of Interleukin-1β Decreases the Severity of Atherosclerosis in ApoE-Deficient Mice

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Kirii, Hirokazu, Niwa, Tamikazu, Yamada, Yasuhiro, Wada, Hisayasu, Saito, Kuniaki, Iwakura, Yoichiro, Asano, Masahide, Moriwaki, Hisataka +1 more·2003·Arteriosclerosis Thrombosis and Vascular Biology

Abstract

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
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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