ArticleMolecular medicine reports2017
PM2.5 exposure decreases viability, migration and angiogenesis in human umbilical vein endothelial cells and human microvascular endothelial cells.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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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Who cites it
11 citing papers in PubMed.
- Impact of Wildfires on Cardiovascular Health.Circulation research · 2024Review
- Wildland fire, air pollution and cardiovascular health: is it time to focus on the microvasculature as a risk assessment tool?Frontiers in physiology · 2023Review
- Adverse effects of air pollution-derived fine particulate matter on cardiovascular homeostasis and disease.Trends in cardiovascular medicine · 2022Review
- Effect modification by sex for associations of fine particulate matter (PMEnvironmental research letters : ERL [Web site] · 2022Article
- Global research trends in atherosclerosis: A bibliometric and visualized study.Frontiers in cardiovascular medicine · 2022Article
- Mechanisms of cardiovascular toxicity induced by PMEnvironmental science and pollution research international · 2021Review
- The critical role of endothelial function in fine particulate matter-induced atherosclerosis.Particle and fibre toxicology · 2020Review
- Elderly Mortality and Exposure to Fine Particulate Matter and Ozone.Journal of Korean medical science · 2019Article
- Effects of Different Components of PMInternational journal of environmental research and public health · 2019Article
- A Review of Recent Advances in Research on PMInternational journal of environmental research and public health · 2018Review
- PMParticle and fibre toxicology · 2018Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have confirmed that exposure to particulate matter with a diameter of ≤2.5 µm (PM2.5) is associated with inflammation. PM2.5 decreases cardiac cell viability and increases apoptosis through overproduction of reactive oxygen species (ROS). In the present study, the role of PM2.5 in ECs was investigated in vitro. Human umbilical vein endothelial cells and human microvascular endothelial cells (ECs) were incubated with PM2.5 (100‑800 µg/ml) to investigate the effects of PM2.5 on EC viability, migration, tube formation and intracellular levels of ROS. Cell viability and cell apoptosis were determined by MTT assay and flow cytometry analysis. Cell migration was assessed using a Boyden chamber assay, and tube formation was determined by matrigel assay. Tumor necrosis factor‑α and interleukin‑8 levels were measured by ELISA, and ROS levels were assessed with 2',7'‑dichlorofluorescin diacetate. The results indicated that PM2.5 decreases EC viability and increases EC apoptosis in a concentration‑dependent manner. PM2.5 also decreased EC tube formation in a dose‑dependent manner. The results also demonstrated that PM2.5 suppresses adhesion to EC extracellular matrix proteins. Furthermore, PM2.5 exposure significantly induced ROS generation, indicative of oxidative stress. Finally, it was demonstrated that PM2.5 decreased angiogenesis in vivo. These results suggested that repeated exposure to PM2.5 induces vascular inflammation.
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