ArticleParticle and fibre toxicology2012
Particulate matter air pollution disrupts endothelial cell barrier via calpain-mediated tight junction protein degradation.
Article in Particle and fibre toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Impact of airborne particulate matter on skin: a systematic review from epidemiology to in vitro studies.Particle and fibre toxicology · 2020Pooled it
- Environmental pollutants and the gut microbiota: mechanistic links from exposure to systemic disease.Frontiers in microbiology · 2026Review
- Therapeutic nanoparticle safety in pregnancy: Bridging knowledge gaps with environmental insights and a translational roadmap.Journal of controlled release : official journal of the Controlled Release Society · 2025Review
- ROS-Activated TRPM2 Channel: Calcium Homeostasis in Cardiovascular/renal System and Speculation in Cardiorenal Syndrome.Cardiovascular drugs and therapy · 2025Review
- Air Pollution and Skin Diseases.Annals of dermatology · 2025Review
- Oxidative stress in ARDS: mechanisms and therapeutic potential.Frontiers in pharmacology · 2025Review
- PMToxicology and applied pharmacology · 2024Article
- Air-Pollution-Mediated Microbial Dysbiosis in Health and Disease: Lung-Gut Axis and Beyond.Journal of xenobiotics · 2024Review
- Cytotoxicity and Epithelial Barrier Toxicity of Fine Particles from Residential Biomass Pellet Burning.Environmental science & technology · 2024Article
- Article
- Spatial Measurement and Inhibition of Calpain Activity in Traumatic Brain Injury with an Activity-Based Nanotheranostic Platform.ACS nano · 2024Article
- Ambient Particulate Matter Induces In Vitro Toxicity to Intestinal Epithelial Cells without Exacerbating Acute Colitis Induced by Dextran Sodium Sulfate or 2,4,6-Trinitrobenzenesulfonic Acid.International journal of molecular sciences · 2024Article
- Review
- The Combination of 5-FU and Resveratrol Can Suppress the Growth of Glioblastoma Cells Through Downregulation of TRPM2 and β-Catenin.Journal of molecular neuroscience : MN · 2024Article
- Calpain Promotes LPS-induced Lung Endothelial Barrier Dysfunction via Cleavage of Talin.American journal of respiratory cell and molecular biology · 2023Article
- Air pollution and respiratory infections: the past, present, and future.Toxicological sciences : an official journal of the Society of Toxicology · 2023Review
- The Road to Malignant Cell Transformation after Particulate Matter Exposure: From Oxidative Stress to Genotoxicity.International journal of molecular sciences · 2023Review
- Article
- Particulate matter promotes the epithelial to mesenchymal transition in human lung epithelial cells via the ROS pathway.American journal of translational research · 2023Article
- Particulate matter increases connexin 43 expression and exacerbates endothelial barrier disruption.American journal of translational research · 2023Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundExposure to particulate matter (PM) is a significant risk factor for increased cardiopulmonary morbidity and mortality. The mechanism of PM-mediated pathophysiology remains unknown. However, PM is proinflammatory to the endothelium and increases vascular permeability in vitro and in vivo via ROS generation.
objectivesWe explored the role of tight junction proteins as targets for PM-induced loss of lung endothelial cell (EC) barrier integrity and enhanced cardiopulmonary dysfunction.
methodsChanges in human lung EC monolayer permeability were assessed by Transendothelial Electrical Resistance (TER) in response to PM challenge (collected from Ft. McHenry Tunnel, Baltimore, MD, particle size >0.1 μm). Biochemical assessment of ROS generation and Ca2+ mobilization were also measured.
resultsPM exposure induced tight junction protein Zona occludens-1 (ZO-1) relocation from the cell periphery, which was accompanied by significant reductions in ZO-1 protein levels but not in adherens junction proteins (VE-cadherin and β-catenin). N-acetyl-cysteine (NAC, 5 mM) reduced PM-induced ROS generation in ECs, which further prevented TER decreases and atteneuated ZO-1 degradation. PM also mediated intracellular calcium mobilization via the transient receptor potential cation channel M2 (TRPM2), in a ROS-dependent manner with subsequent activation of the Ca2+-dependent protease calpain. PM-activated calpain is responsible for ZO-1 degradation and EC barrier disruption. Overexpression of ZO-1 attenuated PM-induced endothelial barrier disruption and vascular hyperpermeability in vivo and in vitro.
conclusionsThese results demonstrate that PM induces marked increases in vascular permeability via ROS-mediated calcium leakage via activated TRPM2, and via ZO-1 degradation by activated calpain. These findings support a novel mechanism for PM-induced lung damage and adverse cardiovascular outcomes.
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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.