ArticleCellular signalling2019
Microtubule destabilization caused by particulate matter contributes to lung endothelial barrier dysfunction and inflammation.
Article in Cellular signalling, 2019. 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, 22 citations in OpenAlex.
- DRD1 downregulation contributes to mechanical stretch-induced lung endothelial barrier dysfunction.Theranostics · 2021Trial
- Microtubules and mechanosensing: key players in endothelial responses to mechanical stimuli.Cellular and molecular life sciences : CMLS · 2025Review
- Differential Effects of HDAC6 Inhibition Versus Knockout During Hepatic Ischemia-Reperfusion Injury Highlight Importance of HDAC6 C-terminal Zinc-finger Ubiquitin-binding Domain.Transplantation · 2024Article
- Soluble pathogenic tau enters brain vascular endothelial cells and drives cellular senescence and brain microvascular dysfunction in a mouse model of tauopathy.Nature communications · 2023Article
- The macrophage senescence hypothesis: the role of poor heat shock response in pulmonary inflammation and endothelial dysfunction following chronic exposure to air pollution.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Impact of Particles on Pulmonary Endothelial Cells.Toxics · 2022Review
- NF-κB-dependent repression of Sox18 transcription factor requires the epigenetic regulators histone deacetylases 1 and 2 in acute lung injury.Frontiers in physiology · 2022Article
- Ruscogenin attenuates particulate matter-induced acute lung injury in mice via protecting pulmonary endothelial barrier and inhibiting TLR4 signaling pathway.Acta pharmacologica Sinica · 2021Article
- Microtubules as Major Regulators of Endothelial Function: Implication for Lung Injury.Frontiers in physiology · 2021Review
- Rho and Reactive Oxygen Species at Crossroads of Endothelial Permeability and Inflammation.Antioxidants & redox signaling · 2019Article
- SOCS3-microtubule interaction via CLIP-170 and CLASP2 is critical for modulation of endothelial inflammation and lung injury.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Exposure to particulate matter (PM) associated with air pollution remains a major public health concern, as it has been linked to significant increase in cardiopulmonary morbidity and mortality. Lung endothelial cell (EC) dysfunction is one of the hallmarks of cardiovascular events of lung exposure to PM. However, the role of PM in acute lung injury (ALI) exacerbation and delayed recovery remains incompletely understood. This study tested a hypothesis that PM augments lung injury and EC barrier dysfunction via microtubule-dependent mechanisms. Our data demonstrate that in pulmonary EC PM caused time- and dose-dependent remodeling of actin cytoskeleton and considerable destabilization of the microtubule (MT) network. These events led to the weakening of cell junctions and formation of actin stress fibers, resulting in disruption of lung EC monolayer and increased permeability. PM also caused ROS-dependent activation of MT-specific deacetylase, HDAC6. Suppression of HDAC6 activity by pharmacological inhibitors or siRNA-based depletion of HDAC6 abolished PM-induced EC permeability increase, which was accompanied by reduced activation of stress kinase signaling, inhibition of Rho cascade, decreased IL-6 production and suppressed activation of its downstream target STAT3. Pretreatment of pulmonary EC with IL-6 inhibitor led to inhibition of STAT3 activity and decreased PM-induced hyper-permeability. Because one of the major activators of Rho-GTPase, GEFH1, is localized on the MT, we examined its involvement in PM-caused EC barrier compromise. Inhibition of GEF-H1 activation significantly attenuated PM-induced permeability increase. Moreover, combined inhibition of IL-6 and GEF-H1 signaling exhibited additive protective effect. Taken together, these results demonstrate a critical involvement of MT-associated signaling in the PM-induced exacerbation of lung EC barrier compromise and inflammatory response.
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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.