ArticleProceedings of the National Academy of Sciences of the United States of America1996
Hypoxia enhances stimulus-dependent induction of E-selectin on aortic endothelial cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 65 citations in OpenAlex.
- CPAP may promote an endothelial inflammatory milieu in sleep apnoea after coronary revascularization.EBioMedicine · 2024Trial
- Oxygen regulation in the earliest animals: spatiotemporal resolution of oxygen dynamics in single-osculumFrontiers in physiology · 2026Article
- SubvertingBiology · 2024Review
- Detrimental interactions of hypoxia and complement MASP-1 in endothelial cells as a model for atherosclerosis-related diseases.Scientific reports · 2024Article
- A microfluidic device for assessment of E-selectin-mediated neutrophil recruitment to inflamed endothelium and prediction of therapeutic response in sickle cell disease.Biosensors & bioelectronics · 2023Article
- Non-circadian aspects of BHLHE40 cellular function in cancer.Genes & cancer · 2020Article
- Tumor Hypoxia Regulates Immune Escape/Invasion: Influence on Angiogenesis and Potential Impact of Hypoxic Biomarkers on Cancer Therapies.Frontiers in immunology · 2020Review
- The transcription factor DEC1 (stra13, SHARP2) is associated with the hypoxic response and high tumour grade in human breast cancers.British journal of cancer · 2004Article
- Ecto-5'-nucleotidase (CD73) regulation by hypoxia-inducible factor-1 mediates permeability changes in intestinal epithelia.The Journal of clinical investigation · 2002Article
- Identification of tumor associated single-chain Fv by panning and screening antibody phage library using tumor cells.World journal of gastroenterology · 2002Article
- Hypoxia-inducible factor 1-dependent induction of intestinal trefoil factor protects barrier function during hypoxia.The Journal of experimental medicine · 2001Article
- Therapeutic targets for hypoxia-elicited pathways.Pharmaceutical research · 1999Review
- Monocyte adhesion and spreading on human endothelial cells is dependent on Rho-regulated receptor clustering.The Journal of cell biology · 1999Article
- Activated endothelial cells elicit paracrine induction of epithelial chloride secretion. 6-Keto-PGF1alpha is an epithelial secretagogue.The Journal of clinical investigation · 1998Article
- Microvascular endothelial cells sustain preadipocyte viability under hypoxic conditions.In vitro cellular & developmental biology. AnimalArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
In many diseases, tissue hypoxia occurs in conjunction with other inflammatory processes. Since previous studies have demonstrated a role for leukocytes in ischemia/reperfusion injury, we hypothesized that endothelial hypoxia may "superinduce" expression of an important leukocyte adhesion molecule, E-selectin (ELAM-1, CD62E). Bovine aortic endothelial monolayers were exposed to hypoxia in the presence or absence of tumor-necrosis factor alpha (TNF-alpha) or lipopolysaccharide (LPS). Cell surface E-selectin was quantitated by whole cell ELISA or by immunoprecipitation using polyclonal anti-E-selectin sera. Endothelial mRNA levels were assessed using ribonuclease protection assays. Hypoxia alone did not induce endothelial E-selectin expression. However, enhanced induction of E-selectin was observed with the combination of hypoxia and TNF-alpha (270% increase over normoxia and TNF-alpha) or hypoxia and LPS (190% increase over normoxia and LPS). These studies revealed that a mechanism for such enhancement may be hypoxia-elicited decrements in endothelial intracellular levels of cAMP (<50% compared with normoxia). Addition of forskolin and isobutyl-methyl-xanthine during hypoxia resulted in reversal of cAMP decreases and a loss of enhanced E-selectin surface expression with the combination of TNF-alpha and hypoxia. We conclude that endothelial hypoxia may provide a novel signal for superinduction of E-selectin during states of inflammation.
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Registered trials
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