ArticleCirculation research2010
Low doses of lipopolysaccharide and minimally oxidized low-density lipoprotein cooperatively activate macrophages via nuclear factor kappa B and activator protein-1: possible mechanism for acceleration of atherosclerosis by subclinical endotoxemia.
Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
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Who cites it
100 citing papers in PubMed, 174 citations in OpenAlex.
- A Single-Cell Analysis Reveals Macrophage Heterogeneity Driving Plaque Vulnerability in Coronary and Carotid Arteries.Journal of atherosclerosis and thrombosis · 2026Article
- Bacterial lipopolysaccharide model of neuroinflammation-associated neurodegeneration in Wistar rats: A comparison between different durations of lipopolysaccharide induction.Veterinary world · 2024Article
- Deciphering the Role of Copper Homeostasis in Atherosclerosis: From Molecular Mechanisms to Therapeutic Targets.International journal of molecular sciences · 2024Review
- Bixin, a New Atheroprotective Carotenoid Candidate, Prevents oxLDL-Induced Cytotoxicity and Mitochondrial Dysfunction in Macrophages: Involvement of the Nrf2 and NF-κB Pathways.Foods (Basel, Switzerland) · 2024Article
- Resolving neutrophils through genetic deletion of TRAM attenuate atherosclerosis pathogenesis.iScience · 2024Article
- Immune Homeostasis Maintenance Through Advanced Immune Therapeutics to Target Atherosclerosis.Methods in molecular biology (Clifton, N.J.) · 2024Article
- LPS adsorption and inflammation alleviation by polymyxin B-modified liposomes for atherosclerosis treatment.Acta pharmaceutica Sinica. B · 2023Article
- Genetic deletion of hepatic NCOR1 protects from atherosclerosis by promoting alternative bile acid-metabolism and sterol excretion.Cardiovascular diabetology · 2023Article
- Skin Cell and Tissue Responses to Cross-Linked Hyaluronic Acid in Low-Grade Inflammatory Conditions.International journal of inflammation · 2023Article
- Anti-malarial artesunate ameliorates atherosclerosis by modulating arterial inflammatory responsesFrontiers in pharmacology · 2023Article
- Circulating Microbiota in Cardiometabolic Disease.Frontiers in cellular and infection microbiology · 2022Review
- Coronary atherosclerosis severity is closely associated with decreased GLP-1R positivity among CD16Atherosclerosis plus · 2021Article
- Two Faces of Macrophages: Training and Tolerance.Biomedicines · 2021Review
- Article
- Circulating Microbial Signatures and Cardiovascular Death in Patients With ESRD.Kidney international reports · 2021Article
- TRAM-Related TLR4 Pathway Antagonized by IRAK-M Mediates the Expression of Adhesion/Coactivating Molecules on Low-Grade Inflammatory Monocytes.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Review
- Macrophage Paired Immunoglobulin-Like Receptor B Deficiency Promotes Peripheral Atherosclerosis in Apolipoprotein E-Deficient Mice.Frontiers in cell and developmental biology · 2021Article
- Article
- Cholesterol 25-hydroxylase (CH25H) as a promoter of adipose tissue inflammation in obesity and diabetes.Molecular metabolism · 2020Article
40 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
rationaleOxidized low-density lipoprotein (LDL) is an important determinant of inflammation in atherosclerotic lesions. It has also been documented that certain chronic infectious diseases, such as periodontitis and chlamydial infection, exacerbate clinical manifestations of atherosclerosis. In addition, low-level but persistent metabolic endotoxemia is often found in diabetic and obese subjects and is induced in mice fed a high-fat diet.
objectiveIn this study, we examined cooperative macrophage activation by low levels of bacterial lipopolysaccharide (LPS) and by minimally oxidized LDL (mmLDL), as a model for subclinical endotoxemia-complicated atherosclerosis. METHODS AND
resultsWe found that both in vitro and in vivo, mmLDL and LPS (Kdo2-LipidA) cooperatively activated macrophages to express proinflammatory cytokines Cxcl2 (MIP-2), Ccl3 (MIP-1alpha), and Ccl4 (MIP-1beta). Importantly, the mmLDL and LPS cooperative effects were evident at a threshold LPS concentration (1 ng/mL) at which LPS alone induced only a limited macrophage response. Analyzing microarray data with a de novo motif discovery algorithm, we found that genes transcribed by promoters containing an activator protein (AP)-1 binding site were significantly upregulated by costimulation with mmLDL and LPS. In a nuclear factor-DNA binding assay, the cooperative effect of mmLDL and LPS costimulation on c-Jun and c-Fos DNA binding, but not on p65 or p50, was dependent on mmLDL-induced activation of extracellular signal-regulated kinase (ERK) 1/2. In addition, mmLDL induced c-Jun N-terminal kinase (JNK)-dependent derepression of AP-1 by removing nuclear receptor corepressor (NCoR) from the chemokine promoters.
conclusionsThe cooperative engagement of AP-1 and nuclear factor (NF)-kappaB by mmLDL and LPS may constitute a mechanism of increased transcription of inflammatory cytokines within atherosclerotic lesions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.