ArticleBritish journal of pharmacology1999
Endothelin-1 enhances neutrophil adhesion to human coronary artery endothelial cells: role of ET(A) receptors and platelet-activating factor.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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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.
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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
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.
- Circulating cell adhesion molecules in systemic sclerosis: a systematic review and meta-analysis.Frontiers in immunology · 2024Pooled it
- Trial
- Advances in Pathophysiology and Novel Therapeutic Strategies for Coronary No-Reflow Phenomenon.Biomedicines · 2025Review
- Neuroinflammation Involving Endothelin-1 and Platelet-Activating Factor Receptors Contributes To Self-Injurious Behaviors Induced by Bay k-8644 in Adolescent Mice.Neurochemical research · 2025Article
- NETosis Drives Blood Pressure Elevation and Vascular Dysfunction in Hypertension.Circulation research · 2024Article
- Capecitabine May Accelerate Atherosclerosis and Causes Acute Myocardial Infarction in the Left Main Trunk.Cureus · 2023Article
- Serum Biomarkers in Connective Tissue Disease-Associated Pulmonary Arterial Hypertension.International journal of molecular sciences · 2023Review
- When natural antibodies become pathogenic: autoantibodies targeted against G protein-coupled receptors in the pathogenesis of systemic sclerosis.Frontiers in immunology · 2023Review
- A targetable 'rogue' neutrophil-subset, [CD11b+DEspR+] immunotype, is associated with severity and mortality in acute respiratory distress syndrome (ARDS) and COVID-19-ARDS.Scientific reports · 2022Article
- "Rogue" [DEspR+CD11b+] neutrophil subset correlates with severity in spontaneous intracerebral hemorrhage.Frontiers in neurology · 2022Article
- DEspRScientific reports · 2021Article
- Neutrophils as Regulators and Biomarkers of Cardiovascular Inflammation in the Context of Abdominal Aortic Aneurysms.Biomedicines · 2021Review
- Increased Neutrophil-Subset Associated With Severity/Mortality In ARDS And COVID19-ARDS Expresses The Dual Endothelin-1/VEGFsignal-Peptide Receptor (DEspR): An Actionable Therapeutic Target.Research square · 2021Article
- Endothelin antagonism and sodium glucose Co-transporter 2 inhibition. A potential combination therapeutic strategy for COVID-19.Pulmonary pharmacology & therapeutics · 2021Review
- The Role of Neutrophils in Hypertension.International journal of molecular sciences · 2020Review
- Immune Dysfunction in Uremia 2020.Toxins · 2020Review
- Association between circulating big endothelin-1 and noncalcified or mixed coronary atherosclerotic plaques.Coronary artery disease · 2019Article
- The endothelin B receptor plays a crucial role in the adhesion of neutrophils to the endothelium in sickle cell disease.Haematologica · 2017Article
- Potential role for ET-2 acting through ETA receptors in experimental colitis in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Article
- First insight into the proteome landscape of the porcine short posterior ciliary arteries: Key signalling pathways maintaining physiologic functions.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The potent coronary vasoconstrictor, endothelin-1 (ET-1) may also regulate neutrophil traffic into tissues. The aim of the present study was to characterize the endothelin receptors responsible and to investigate the underlying mechanisms. 2. ET-1 (1 nM - 1 microM) markedly enhanced attachment of human neutrophils to lipopolysaccharide-, and to a lesser extent, to ET-1-activated human coronary artery endothelial cells (HCAEC). This can partially be blocked by monoclonal antibodies against E-selectin, L-selectin or CD18, whereas combination of the three antibodies inhibited adhesion by approximately 83%. Increases in neutrophil adhesion evoked by ET-1 were also blocked by the platelet-activating factor (PAF) antagonists, BN 52021 (50 microM) and WEB 2086 (10 microM). 3. ET-1 downregulated the expression of L-selectin and upregulated expression of CD11b/CD18 and CD45 on the neutrophil surface and induced gelatinase release with EC50 values of approximately 2 nM. These actions of ET-1 were almost completely prevented by the ET(A) receptor antagonist FR 139317 (1 microM) and the ET(A)/ET(B) receptor antagonist bosentan (10 microM), whereas the ET(B) receptor antagonist BQ 788 (1 microM) had no effect. ET-1 slightly increased the expression of E-selectin and ICAM-1 on HCAEC, that was prevented by BQ 788, but not by FR 139317. 4. Receptor binding studies indicated the presence of ET(B) receptors (KD: 40 pM) on phosphoramidon-treated HCAEC and the predominant expression of ET(A) receptors (KD: 38 pM) on neutrophils. 5. These results indicate that promotion by ET-1 of neutrophil adhesion to HCAEC is predominantly mediated through activation of ET(A) receptors on neutrophils and subsequent generation of PAF.
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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 Socratic graph.