ArticleAmerican journal of physiology. Cell physiology2013
Atmospheric ultrafine particles promote vascular calcification via the NF-κB signaling pathway.
Article in American journal of physiology. Cell physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- The role of macrophages in vascular calcification: strategies for diagnosis and treatment.Frontiers in immunology · 2025Review
- Dissecting the multifaceted roles of autophagy in cancer initiation, growth, and metastasis: from molecular mechanisms to therapeutic applications.Medical oncology (Northwood, London, England) · 2024Review
- Integrating 4-D light-sheet fluorescence microscopy and genetic zebrafish system to investigate ambient pollutants-mediated toxicity.The Science of the total environment · 2023Review
- The bio-distribution, clearance pathways, and toxicity mechanisms of ambient ultrafine particles.Eco-Environment & Health · 2023Review
- Wildland fire, air pollution and cardiovascular health: is it time to focus on the microvasculature as a risk assessment tool?Frontiers in physiology · 2023Review
- Inflammation: a putative link between phosphate metabolism and cardiovascular disease.Clinical science (London, England : 1979) · 2021Review
- The Cell Origin and Role of Osteoclastogenesis and Osteoblastogenesis in Vascular Calcification.Frontiers in cardiovascular medicine · 2021Review
- Integrating systematic biological and proteomics strategies to explore the pharmacological mechanism of danshen yin modified on atherosclerosis.Journal of cellular and molecular medicine · 2020Article
- Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma.International journal of molecular sciences · 2020Review
- Diesel Exhaust Induces Mitochondrial Dysfunction, Hyperlipidemia, and Liver Steatosis.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Thyroxine Affects Lipopolysaccharide-Induced Macrophage Differentiation and Myocardial Cell Apoptosis via the NF-Mediators of inflammation · 2019Article
- Ma Xing Shi Gan Decoction Attenuates PM2.5 Induced Lung Injury via Inhibiting HMGB1/TLR4/NFκB Signal Pathway in Rat.Frontiers in pharmacology · 2019Article
- Selenoprotein S inhibits inflammation-induced vascular smooth muscle cell calcification.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2018Article
- Transcriptional profiling of human bronchial epithelial cell BEAS-2B exposed to diesel and biomass ultrafine particles.BMC genomics · 2018Article
- A critical review of assays for hazardous components of air pollution.Free radical biology & medicine · 2018Review
- Lipopolysaccharide attached to urban particulate matter 10 suppresses immune responses in splenocytes while particulate matter itself activates NF-κB.Toxicology research · 2016Article
- Immunotoxicological impact of occupational and environmental nanoparticles exposure: The influence of physical, chemical, and combined characteristics of the particles.International journal of immunopathology and pharmacology · 2016Review
- Ambient ultrafine particles reduce endothelial nitric oxide production via S-glutathionylation of eNOS.Biochemical and biophysical research communications · 2013Article
- Ambient ultrafine particles alter lipid metabolism and HDL anti-oxidant capacity in LDLR-null mice.Journal of lipid research · 2013Article
- Evaluation of in vitro cytoxicity and genotoxicity of size-fractionated air particles sampled during road tunnel construction.BioMed research international · 2013Article
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Authors and funding
9 authors.
Funding
Abstract
Exposure to atmospheric fine particulate matter (PM(2.5)) is a modifiable risk factor of cardiovascular disease. Ultrafine particles (UFP, diameter <0.1 μm), a subfraction of PM(2.5), promote vascular oxidative stress and inflammatory responses. Epidemiologic studies suggest that PM exposure promotes vascular calcification. Here, we assessed whether UFP exposure promotes vascular calcification via NF-κB signaling. UFP exposure at 50 μg/ml increased alkaline phosphatase (ALP) activity by 4.4 ± 0.2-fold on day 3 (n = 3, P < 0.001) and matrix calcification by 3.5 ± 1.7-fold on day 10 (n = 4, P < 0.05) in calcifying vascular cells (CVC), a subpopulation of vascular smooth muscle cells with osteoblastic potential. Treatment of CVC with conditioned media derived from UFP-treated macrophages (UFP-CM) also led to an increase in ALP activities and matrix calcification. Furthermore, both UFP and UFP-CM significantly increased NF-κB activity, and cotreatment with an NF-κB inhibitor, JSH23, attenuated both UFP- and UFP-CM-induced ALP activity and calcification. When low-density lipoprotein receptor-null mice were exposed to UFP at 359.5 μg/m(3) for 10 wk, NF-κB activation and vascular calcification were detected in the regions of aortic roots compared with control filtered air-exposed mice. These findings suggest that UFP promotes vascular calcification via activating NF-κB signaling.
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