ArticlePloS one2013
Cyclooxygenase-1 and prostacyclin production by endothelial cells in the presence of mild oxidative stress.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 31 citations in OpenAlex.
- Potential Role of Polyphenols in Platelet Aggregation and Blood Coagulation.Journal of cardiovascular development and disease · 2026Review
- In Vitro Effects of Minor Olive Oil Compounds on Prostacyclin/Thromboxane Balance Under Acute High-Glucose Conditions.Biomolecules · 2026Article
- Therapeutic Effects of Green Tea Polyphenol (‒)-Epigallocatechin-3-Gallate (EGCG) in Relation to Molecular Pathways Controlling Inflammation, Oxidative Stress, and Apoptosis.International journal of molecular sciences · 2022Review
- Biological Effects of EGCG@MOF Zn(BTC)Molecules (Basel, Switzerland) · 2022Article
- Vascular Dysfunction in Preeclampsia.Cells · 2021Review
- Extracellular adenosine enhances the ability of PMNs to kill Streptococcus pneumoniae by inhibiting IL-10 production.Journal of leukocyte biology · 2020Article
- Green Tea Extracts Epigallocatechin-3-gallate for Different Treatments.BioMed research international · 2017Review
- Augmented oxidative stress and preserved vasoconstriction induced by hydrogen peroxide in coronary arteries in obesity: role of COX-2.British journal of pharmacology · 2016Article
- The role of valvular endothelial cell paracrine signaling and matrix elasticity on valvular interstitial cell activation.Biomaterials · 2014Article
- New insights into the mechanisms of polyphenols beyond antioxidant properties; lessons from the green tea polyphenol, epigallocatechin 3-gallate.Redox biology · 2014Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed at evaluating the relative contribution of endothelial cyclooxygenase-1 and -2 (COX-1 and COX-2) to prostacyclin (PGI(2)) production in the presence of mild oxidative stress resulting from autooxidation of polyphenols such as (-)-epigallocatechin 3-gallate (EGCG), using both endothelial cells in culture and isolated blood vessels. EGCG treatment resulted in an increase in hydrogen peroxide formation in human umbilical vein endothelial cells. In the presence of exogenous arachidonic acid and EGCG, PGI(2) production was preferentially inhibited by a selective COX-1 inhibitor. This effect of selective inhibition was also substantially reversed by catalase. In addition, EGCG caused vasorelaxation of rat aortic ring only partially abolished by a nitric oxide synthase inhibitor. Concomitant treatment with a selective COX-1 inhibitor completely prevented the vasorelaxation as well as the increase in PGI(2) accumulation in the perfusate observed in EGCG-treated aortic rings, while a selective COX-2 inhibitor was completely uneffective. Our data strongly support the notions that H(2)O(2) generation affects endothelial PGI(2) production, making COX-1, and not COX-2, the main source of endothelial PGI(2) under altered oxidative tone conditions. These results might be relevant to the reappraisal of the impact of COX inhibitors on vascular PGI(2) production in patients undergoing significant oxidative stress.
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