Cited by 1,019Atherosclerosis and Cardiovascular DiseasesCholesterol and Lipid MetabolismImmune Response and Inflammation

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Lack of Toll-like receptor 4 or myeloid differentiation factor 88 reduces atherosclerosis and alters plaque phenotype in mice deficient in apolipoprotein E

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Michelsen, Kathrin S., Wong, Michelle H., Shah, Prediman K., Zhang, Wenxuan, Yano, Juliana, Doherty, Terence M., Akira, Shizuo, Rajavashisth, Tripathi B., Arditi, Moshe·2004·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.0403249101PMC PMC489994

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Abstract

Toll-like receptors (TLRs) and the downstream adaptor molecule myeloid differentiation factor 88 (MyD88) play an essential role in the innate immune responses. Here, we demonstrate that genetic deficiency of TLR4 or MyD88 is associated with a significant reduction of aortic plaque areas in atherosclerosis-prone apolipoprotein E-deficient mice, despite persistent hypercholesterolemia, implying an important role for the innate immune system in atherogenesis. Apolipoprotein E-deficient mice that also lacked TLR4 or MyD88 demonstrated reduced aortic atherosclerosis that was associated with reductions in circulating levels of proinflammatory cytokines IL-12 or monocyte chemoattractant protein 1, plaque lipid content, numbers of macrophage, and cyclooxygenase 2 immunoreactivity in their plaques. Endothelial-leukocyte adhesion in response to minimally modified low-density lipoprotein was reduced in aortic endothelial cells derived from MyD88-deficient mice. Taken together, our results suggest an important role for TLR4 and MyD88 signaling in atherosclerosis in a hypercholesterolemic mouse model, providing a pathophysiologic link between innate immunity, inflammation, and atherogenesis.

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Authors: Michelsen, K. S., Wong, M. H., Shah, P. K., Zhang, W., Yano, J., Doherty, T. M., Akira, S., Rajavashisth, T. B., & Arditi, M.
Affiliations: Cedars-Sinai Medical Center (US)
Corresponding author: Arditi, Moshe
ORCID: Michelsen, Kathrin S.
Shah, Prediman K.
Zhang, Wenxuan
Doherty, Terence M.
Akira, Shizuo
Arditi, Moshe
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2004-07-12
Volume: 101
Issue: 29
Pages: 10679-10684
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.0403249101
PMC: PMC489994
OpenAlex: W2018788678
Cited by: 1,019
References: 57
Citations by year: 2026: 20 · 2025: 17 · 2024: 25 · 2023: 25 · 2022: 35 · 2021: 21 · 2020: 36 · 2019: 52 · 2018: 36 · 2017: 37 · 2016: 43 · 2015: 64 · 2014: 53 · 2013: 68 · 2012: 68
FWCI: 18.10
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r01hl058555-04)
National Heart, Lung, and Blood Institute (HL66436, HL 58555, R01HL066436, R29HL051980, HL 51980, R01HL051980)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords: TLR4, MyD88, atherosclerosis, apolipoprotein E deficiency, innate immunity, atherogenesis, aortic plaque, hypercholesterolemia, inflammatory cytokines, IL-12, MCP-1, macrophages, cyclooxygenase-2, plaque inflammation
MeSH terms: Animals, Antigens, Differentiation, Aorta, Apolipoproteins E, Arteriosclerosis, Cells, Cultured, Female, Humans, Immunity, Innate, Isoenzymes, Lipids, Macrophages, Male, Membrane Glycoproteins, Membrane Proteins, Mice, Inbred C57BL, Phenotype, Prostaglandin-Endoperoxide Synthases, Receptors, Cell Surface, Receptors, Immunologic, Signal Transduction, Mice, Knockout, Interleukin-12, Chemokine CCL2, Endothelial Cells, Adaptor Proteins, Signal Transducing, Lipid Metabolism, Toll-Like Receptors, Toll-Like Receptor 4, Mice, Cyclooxygenase 2, Myeloid Differentiation Factor 88

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Lack of Toll-like receptor 4 or myeloid differentiation factor 88 reduces atherosclerosis and alters plaque phenotype in mice deficient in apolipoprotein E

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