ArticlePulmonary circulation
Particulate matter disrupts human lung endothelial cell barrier integrity via Rho-dependent pathways.
Article in Pulmonary circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 42 citations in OpenAlex.
- Article
- Molecular mechanisms of air pollution-induced carcinogenesis and the emerging role of microplastics.Human genomics · 2025Review
- Inhibitory Effects of 3-Deoxysappanchalcone on Particulate-Matter-Induced Pulmonary Injury.Current issues in molecular biology · 2025Article
- The Road to Malignant Cell Transformation after Particulate Matter Exposure: From Oxidative Stress to Genotoxicity.International journal of molecular sciences · 2023Review
- Particulate matter promotes the epithelial to mesenchymal transition in human lung epithelial cells via the ROS pathway.American journal of translational research · 2023Article
- Effect of Quercetin on mitoBKInternational journal of molecular sciences · 2022Article
- Serum peptidome: diagnostic window into pathogenic processes following occupational exposure to carbon nanomaterials.Particle and fibre toxicology · 2021Article
- Activation of mTOR mediates hyperglycemia-induced renal glomerular endothelial hyperpermeability via the RhoA/ROCK/pMLC signaling pathway.Diabetology & metabolic syndrome · 2021Article
- The critical role of endothelial function in fine particulate matter-induced atherosclerosis.Particle and fibre toxicology · 2020Review
- Prognostic value of aberrantly expressed methylation genes in human hepatocellular carcinoma.Bioscience reports · 2020Article
- P53 Regulates the Redox Status of Lung Endothelial Cells.Inflammation · 2020Article
- Biapenem as a Novel Insight into Drug Repositioning against Particulate Matter-Induced Lung Injury.International journal of molecular sciences · 2020Article
- The Enigma of Endothelium in COVID-19.Frontiers in physiology · 2020Article
- Deciphering the Code between Air Pollution and Disease: The Effect of Particulate Matter on Cancer Hallmarks.International journal of molecular sciences · 2019Review
- Microtubule destabilization caused by particulate matter contributes to lung endothelial barrier dysfunction and inflammation.Cellular signalling · 2019Article
- Respirable Uranyl-Vanadate-Containing Particulate Matter Derived From a Legacy Uranium Mine Site Exhibits Potentiated Cardiopulmonary Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Fine Particulate Matter Pollution and Risk of Community-Acquired Sepsis.International journal of environmental research and public health · 2018Article
- Role of truncated oxidized phospholipids in acute endothelial barrier dysfunction caused by particulate matter.PloS one · 2018Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Increased exposure to ambient particulate matter (PM) is associated with elevated morbidity and mortality in patients with cardiopulmonary diseases and cancer. We and others have shown that PM induces lung microvascular barrier dysfunction which potentially enhances the systemic toxicity of PM. However, the mechanisms by which PM disrupts vascular endothelial integrity remain incompletely explored. We hypothesize that PM induces endothelial cell (EC) cytoskeleton rearrangement via Rho GTPase-dependent pathways to facilitate vascular hyperpermeability. Fine PM induced time-dependent activation of cytoskeletal machinery with increases in myosin light chain (MLC) phosphorylation and EC barrier disruption measured by transendothelial electrical resistance (TER), events attenuated by the Rho-dependent kinase (ROCK) inhibitor Y-27632 or the reactive oxygen species (ROS) scavenger, N-acetylcysteine (NAC). Both Y-27632 and NAC prevented PM-induced stress fiber formation and phospho-MLC accumulation in human lung ECs. PM promotes rapid accumulation of Rho-GTP. This event is attenuated by NAC or knockdown of RhoA (siRNA). Consistent with ROCK activation, PM induced phosphorylation of myosin light chain phosphatase (MYPT) at Thr850, a post-translational modification known to inhibit phosphatase activity. Furthermore, PM activates the guanine nucleotide exchange factor (GEF) for Rho, p115, with p115 translocation to the cell periphery, in a ROS-dependent manner. Together these results demonstrate that fine PM induces EC cytoskeleton rearrangement via Rho-dependent pathways that are dependent upon the generation of oxidative stress. As the disruption of vascular integrity further contributes to cardiopulmonary physiologic derangements, these findings provide pharmacologic targets for prevention of PM-induced cardiopulmonary toxicity.
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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.