ArticleLung
Release of soluble E-selectin from activated endothelial cells upon apoptosis.
Article in Lung. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The trial behind it
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Endothelial injury and inflammation in patients with hyperuricemic nephropathy at chronic kidney disease stages 1-2 and 3-4.World journal of clinical cases · 2022Trial
- Pathophysiological mechanisms and therapeutic potential of E-selectin in pulmonary arterial hypertension.Frontiers in immunology · 2026Review
- Cytocompatibility Evaluation of PEG-Methylsulfone Hydrogels.ACS omega · 2023Article
- Evaluation of admission levels of P, E and L selectins as predictors for thrombosis in hospitalized COVID-19 patients.Clinical and experimental medicine · 2022Article
- A nanozyme-based competitive electrochemical immunosensor for the determination of E-selectin.Mikrochimica acta · 2022Article
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- A Novel Subset of CD95Frontiers in immunology · 2020Article
- Quinic Acid-Conjugated Nanoparticles Enhance Drug Delivery to Solid Tumors via Interactions with Endothelial Selectins.Small (Weinheim an der Bergstrasse, Germany) · 2018Article
- Both MC1 and MC3 Receptors Provide Protection From Cerebral Ischemia-Reperfusion-Induced Neutrophil Recruitment.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Soluble adhesion molecules as markers for sepsis and the potential pathophysiological discrepancy in neonates, children and adults.Critical care (London, England) · 2014Review
- Glucose and fatty acid metabolism in a 3 tissue in-vitro model challenged with normo- and hyperglycaemia.PloS one · 2012Article
- Endothelial activation and circulating markers of endothelial activation in kidney disease.Nature reviews. Nephrology · 2010Review
- Retinal endothelial cell apoptosis stimulates recruitment of endothelial progenitor cells.Investigative ophthalmology & visual science · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Circulating soluble E-selectin is increased in diseases associated with endothelial apoptosis such as sepsis and acute respiratory distress syndrome. We investigated the mechanism by which endothelial cell (EC) apoptosis may promote soluble E-selectin release. We found that serum deprivation of EC caused apoptosis, yet it did not induce E-selectin EC surface expression. Tumor necrosis factor-alpha (TNFalpha) significantly increased EC E-selectin surface expression. Soluble E-selectin was noted, however, only in the medium of TNFalpha-activated, apoptotic EC. Preincubation of the EC with the caspase inhibitor z-VAD-fmk significantly attenuated soluble E-selectin levels in the culture medium of TNFalpha-activated, apoptotic EC, but it had no effect on E-selectin surface expression. These results indicate that TNFalpha activation, but not apoptosis, is necessary for E-selectin surface expression in EC. Furthermore, E-selectin release from EC requires caspase-3 activation. Thus, increased concentrations of circulating E-selectin in serum may serve as a marker for endothelial apoptosis in certain disease states.
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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.