ArticleToxicological sciences : an official journal of the Society of Toxicology2014
Air pollution upregulates endothelial cell procoagulant activity via ultrafine particle-induced oxidant signaling and tissue factor expression.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 38 citations in OpenAlex.
- A cell-based model to study mechanisms of endothelial-dependent thrombin generation in response to inflammation and its modulation by hydroxychloroquine.Research and practice in thrombosis and haemostasis · 2025Article
- The cardiovascular effects of air pollution: Prevention and reversal by pharmacological agents.Pharmacology & therapeutics · 2022Review
- Effect of urban air pollution on CRP and coagulation: a study on inpatients with acute exacerbation of chronic obstructive pulmonary disease.BMC pulmonary medicine · 2021Article
- Clinical Manifestations and Changes of Haematological Markers among Active People Living in Polluted City: The Case of Douala, Cameroon.International journal of environmental research and public health · 2021Article
- Immune biomarkers link air pollution exposure to blood pressure in adolescents.Environmental health : a global access science source · 2020Article
- Review
- Oxidative stress and the cardiovascular effects of air pollution.Free radical biology & medicine · 2020Review
- Reactive Oxygen Species in Venous Thrombosis.International journal of molecular sciences · 2020Review
- Ultrafine particulate matter exposure impairs vasorelaxant response in superoxide dismutase 2-deficient murine aortic rings.Journal of toxicology and environmental health. Part A · 2018Article
- Effects of air pollution on human health and practical measures for prevention in Iran.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2016Review
- Air pollution and its effects on lung health in never-smoker youth of Delhi NCR versus Pauri Garhwal: a comparative cross-sectional study.Medical journal, Armed Forces IndiaArticle
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Air pollution exposure is associated with cardiovascular events triggered by clot formation. Endothelial activation and initiation of coagulation are pathophysiological mechanisms that could link inhaled air pollutants to vascular events. Here we investigated the underlying mechanisms of increased endothelial cell procoagulant activity following exposure to soluble components of ultrafine particles (soluble UF). Human coronary artery endothelial cells (HCAEC) were exposed to soluble UF and assessed for their ability to trigger procoagulant activity in platelet-free plasma. Exposed HCAEC triggered earlier thrombin generation and faster fibrin clot formation, which was abolished by an anti-tissue factor (TF) antibody, indicating TF-dependent effects. Soluble UF exposure increased TF mRNA expression without compensatory increases in key anticoagulant proteins. To identify early events that regulate TF expression, we measured endothelial H2O2 production following soluble UF exposure and identified the enzymatic source. Soluble UF exposure increased endothelial H2O2 production, and antioxidants attenuated UF-induced upregulation of TF, linking the procoagulant responses to reactive oxygen species (ROS) formation. Chemical inhibitors and RNA silencing showed that NOX-4, an important endothelial source of H2O2, was involved in UF-induced upregulation of TF mRNA. These data indicate that soluble UF exposure induces endothelial cell procoagulant activity, which involves de novo TF synthesis, ROS production, and the NOX-4 enzyme. These findings provide mechanistic insight into the adverse cardiovascular effects associated with air pollution exposure.
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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.