ArticleAmerican journal of respiratory cell and molecular biology2012
Oxidative stress contributes to lung injury and barrier dysfunction via microtubule destabilization.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 143 citations in OpenAlex.
- Trial
- Reconfiguration of the Microtubule Network and Dynamics in Hypoxic Cancer Cells.Chemical & biomedical imaging · 2026Article
- Mechanosensitive FHL2 tunes endothelial function via microtubule-actomyosin crosstalk.The EMBO journal · 2026Article
- Inflammation-driven mitochondrial dysfunction and ROS accumulation orchestrate pulmonary fibrotic remodeling in sepsis.Redox biology · 2026Article
- Paclitaxel-induced tubulin dysfunction stalls parasite development: synergistic potential with artemisinin against resistant strains.Microbiology spectrum · 2026Article
- Mechanism of Gzma-mediated GEF-H1 activation in intestinal epithelial cells leading to intestinal barrier dysfunction in sepsis.Clinical and translational medicine · 2026Article
- Characterization of woodsmoke generated in the air pollution exposure lab and comparison to diesel exhaust.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Therapeutic targeting of endothelial calcium signaling accelerates the resolution of lung injury.Signal transduction and targeted therapy · 2025Article
- The potential role of hydrogen sulfide-autophagy axis in diseases.Journal of physiology and biochemistry · 2025Review
- Guanine Nucleotide Exchange Factors and Small GTPases: Their Regulation and Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- Pedunculoside alleviates lipopolysaccharide-induced acute lung injury/acute respiratory distress syndrome by inhibiting NF-κB pathway.Scientific reports · 2025Article
- Rhein Mitigates Lung Injury in Severe Acute Pancreatitis Through the Inhibition of MARK4-Mediated Microtubule Destabilization.Journal of inflammation research · 2025Article
- Investigating the protective effects of fluvoxamine against sepsis-related acute lung injury through antiapoptotic, anti-inflammatory, and anti-oxidant features in rats.Iranian journal of basic medical sciences · 2025Article
- Diesel exhaust particle inhalation in conjunction with high-fat diet consumption alters the expression of pulmonary SARS-COV-2 infection pathways, which is mitigated by probiotic treatment in C57BL/6 male mice.Particle and fibre toxicology · 2024Article
- Review
- Building a human lung from pluripotent stem cells to model respiratory viral infections.Respiratory research · 2024Review
- Mechanisms of pulmonary endothelial barrier dysfunction in acute lung injury and acute respiratory distress syndrome.Chinese medical journal pulmonary and critical care medicine · 2024Article
- SFX-01 in hospitalised patients with community-acquired pneumonia during the COVID-19 pandemic: a double-blind, randomised, placebo-controlled trial.ERJ open research · 2024Article
- Regulation of Microtubule Stability in Pulmonary Microvascular Endothelial Cells in Rats with Severe Acute Pancreatitis: Qingyi Decoction is a Potential CDK5 Inhibitor.Journal of inflammation research · 2024Article
- Pathophysiological and Clinical Significance ofToxins · 2023Article
28 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress is an important part of host innate immune response to foreign pathogens, such as bacterial LPS, but excessive activation of redox signaling may lead to pathologic endothelial cell (EC) activation and barrier dysfunction. Microtubules (MTs) play an important role in agonist-induced regulation of vascular endothelial permeability, but their impact in modulation of inflammation and EC barrier has not been yet investigated. This study examined the effects of LPS-induced oxidative stress on MT dynamics and the involvement of MTs in the LPS-induced mechanisms of Rho activation, EC permeability, and lung injury. LPS treatment of pulmonary vascular EC induced elevation of reactive oxygen species (ROS) and caused oxidative stress associated with EC hyperpermeability, cytoskeletal remodeling, and formation of paracellular gaps, as well as activation of Rho, p38 stress kinase, and NF-κB signaling, the hallmarks of endothelial barrier dysfunction. LPS also triggered ROS-dependent disassembly of the MT network, leading to activation of MT-dependent signaling. Stabilization of MTs with epothilone B, or inhibition of MT-associated guanine nucleotide exchange factor (GEF)-H1 activity by silencing RNA-mediated knockdown, suppressed LPS-induced EC barrier dysfunction in vitro, and attenuated vascular leak and lung inflammation in vivo. LPS disruptive effects were linked to activation of Rho signaling caused by LPS-induced MT disassembly and release of Rho-specific GEF-H1 from MTs. These studies demonstrate, for the first time, the mechanism of ROS-induced Rho activation via destabilization of MTs and GEF-H1-dependent activation of Rho signaling, leading to pulmonary EC barrier dysfunction and exacerbation of LPS-induced inflammation.
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