ArticleJournal of immunology (Baltimore, Md. : 1950)2004
Regulation of endotoxin-induced proinflammatory activation in human coronary artery cells: expression of functional membrane-bound CD14 by human coronary artery smooth muscle cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Polymorphisms of the LTA gene may contribute to the risk of myocardial infarction: a meta-analysis.PloS one · 2014Pooled it
- The Oral Microbiome, Oral Hyperpermeability, and Periodontitis in Metabolic Syndrome.Advances in experimental medicine and biology · 2026Review
- CD14 Blockade Modulates Macrophage-Mediated Immunological Injury in a Translational Model of Reperfused ST-Segment Elevation Myocardial Infarction.JACC. Basic to translational science · 2025Article
- Berberine and its derivatives: mechanisms of action in myocardial vascular endothelial injury - a review.Frontiers in pharmacology · 2025Review
- Soluble CD14 and Incident Diabetes Risk: The REasons for Geographic and Racial Differences in Stroke (REGARDS) Study.Journal of the Endocrine Society · 2024Article
- Hyperglycaemia Aggravates Oxidised Low-Density Lipoprotein-Induced Schwann Cell Death via Hyperactivation of Toll-like Receptor 4.Neurology international · 2024Article
- Atherosclerosis and Toll-Like Receptor4 (TLR4), Lectin-Like Oxidized Low-Density Lipoprotein-1 (LOX-1), and Proprotein Convertase Subtilisin/Kexin Type9 (PCSK9).Mediators of inflammation · 2024Review
- The role of serum circulating microbial toxins in severity and cytokine storm of COVID positive patients.Microbial pathogenesis · 2023Review
- The Intriguing Role of TLR Accessory Molecules in Cardiovascular Health and Disease.Frontiers in cardiovascular medicine · 2022Review
- Dysregulation and imbalance of innate and adaptive immunity are involved in the cardiomyopathy progression.Frontiers in cardiovascular medicine · 2022Article
- Cynarin attenuates LPS-induced endothelial inflammation via upregulation of the negative regulator MKP-3.Animal cells and systems · 2022Article
- Cardiovascular Health and The Intestinal Microbial Ecosystem: The Impact of Cardiovascular Therapies on The Gut Microbiota.Microorganisms · 2021Review
- Could Perturbation of Gut Microbiota Possibly Exacerbate the Severity of COVID-19Frontiers in immunology · 2020Review
- Toll-Like Receptor 4 and Inflammatory Micro-Environment of Pancreatic Islets in Type-2 Diabetes Mellitus: A Therapeutic Perspective.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Review
- MiR-590 Inhibits Endothelial Cell Apoptosis by Inactivating the TLR4/NF-κB Pathway in Atherosclerosis.Yonsei medical journal · 2019Article
- Molecular markers relevant to myocardial injury following dental extraction in patients with or without coronary artery disease.BDJ open · 2019Article
- DC-SIGN and Toll-like receptor 4 mediate oxidized low-density lipoprotein-induced inflammatory responses in macrophages.Scientific reports · 2017Article
- Lipopolysaccharide induced vascular smooth muscle cells proliferation: A new potential therapeutic target for proliferative vascular diseases.Cell proliferation · 2017Review
- Biological and Nutritional Properties of Palm Oil and Palmitic Acid: Effects on Health.Molecules (Basel, Switzerland) · 2015Review
- The gut microbiome, kidney disease, and targeted interventions.Journal of the American Society of Nephrology : JASN · 2014Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
Abstract
Low-level endotoxemia has been identified as a powerful risk factor for atherosclerosis. However, little is known about the mechanisms that regulate endotoxin responsiveness in vascular cells. We conducted experiments to compare the relative responses of human coronary artery endothelial cells (HCAEC) and smooth muscle cells (HCASMC) to very low levels of endotoxin, and to elucidate the mechanisms that regulate endotoxin responsiveness in vascular cells. Endotoxin (</=1 ng/ml) caused production of chemotactic cytokines in HCAEC. Endotoxin-induced cytokine production was maximal at LPS-binding protein:soluble CD14 ratios <1, typically observed in individuals with subclinical infection; higher LPS-binding protein:soluble CD14 ratios were inhibitory. Endotoxin potently activated HCASMC, with cytokine release >10-fold higher in magnitude at >10-fold lower threshold concentrations (10-30 pg/ml) compared with HCAEC. This remarkable sensitivity of HCASMC to very low endotoxin concentrations, comparable to that found in circulating monocytes, was not due to differential expression of TLR4, which was detected in HCAEC, HCASMC, and intact coronary arteries. Surprisingly, membrane-bound CD14 was detected in seven different lines of HCASMC, conferring responsiveness to endotoxin and to lipoteichoic acid, a product of Gram-positive bacteria, in these cells. These results suggest that the low levels of endotoxin associated with increased risk for atherosclerosis are sufficient to produce inflammatory responses in coronary artery cells. Because CD14 recognizes a diverse array of inflammatory mediators and functions as a pattern recognition molecule in inflammatory cells, expression of membrane-bound CD14 in HCASMC implies a potentially broader role for these cells in transducing innate immune responses in the vasculature.
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What OpenQuestion holds
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.