ArticleAmerican journal of respiratory cell and molecular biology2016
Cigarette Smoke Disrupted Lung Endothelial Barrier Integrity and Increased Susceptibility to Acute Lung Injury via Histone Deacetylase 6.
Article in American journal of respiratory cell and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 80 citations in OpenAlex.
- DRD1 downregulation contributes to mechanical stretch-induced lung endothelial barrier dysfunction.Theranostics · 2021Trial
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- USP19 facilitates CSE-induced cell damage and ferroptosis in chronic obstructive pulmonary disease by deubiquitinating HDAC6 to drive PRDX6 deacetylation.Immunologic research · 2026Article
- The respiratory health effects of heated tobacco product aerosols in a primary human airway epithelial cell model.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2026Article
- Modelling cigarette smoke-induced lung vascular dysfunction using an alveolus-on-chip.Materials today. Bio · 2026Article
- Association between the endothelial activation and stress index and 28-day all-cause mortality in critically ill patients with chronic obstructive pulmonary disease: a retrospective cohort study and predictive model establishment based on machine learning.BMC pulmonary medicine · 2026Article
- Short-term cigarette smoke exposure aggravates oxidative stress and airway inflammation induced by lipopolysaccharides.Frontiers in physiology · 2026Article
- Integrative single-cell RNA and ATAC sequencing reveals the impact of chronic cigarette smoking on lung epithelial responses to influenza and hyperoxia.Respiratory research · 2025Article
- Oxidative Stress and Inflammation in Hypoxemic Respiratory Diseases and Their Comorbidities: Molecular Insights and Diagnostic Advances in Chronic Obstructive Pulmonary Disease and Sleep Apnea.Antioxidants (Basel, Switzerland) · 2025Review
- Tubulin Acetylation and the Cellular Mechanosensing and Stress Response.Results and problems in cell differentiation · 2025Review
- Cigarette smoke alters calcium flux to induce PP2A membrane trafficking and endothelial cell permeability.Scientific reports · 2024Article
- Ketamine impairs growth cone and synaptogenesis in human GABAergic projection neurons via GSK-3β and HDAC6 signaling.Molecular psychiatry · 2024Article
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
- HDAC6-selective inhibitor CAY10603 ameliorates cigarette smoke-induced small airway remodeling by regulating epithelial barrier dysfunction and reversing.Respiratory research · 2024Article
- Zinc-Dependent Histone Deacetylases in Lung Endothelial Pathobiology.Biomolecules · 2024Review
- Advances in the Mechanistic Study of the Control of Oxidative Stress Injury by Modulating HDAC6 Activity.Cell biochemistry and biophysics · 2023Article
- NLRP3 inflammasome activation in cigarette smoke priming for Pseudomonas aeruginosa-induced acute lung injury.Redox biology · 2022Article
- CIGARETTE SMOKING INCREASES THE RISK OF ACUTE RESPIRATORY DISTRESS SYNDROME.Transactions of the American Clinical and Climatological Association · 2022Article
- 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
- HDAC6: A Neglected Player in Chronic Obstructive Pulmonary Disease?American journal of respiratory cell and molecular biology · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Epidemiologic evidence indicates that cigarette smoke (CS) is associated with the development of acute lung injury (ALI). We have previously shown that brief CS exposure exacerbates lipopolysaccharide (LPS)-induced ALI in vivo and endothelial barrier dysfunction in vitro. In this study, we found that CS also exacerbated Pseudomonas-induced ALI in mice. We demonstrated that lung microvascular endothelial cells (ECs) isolated from mice exposed to CS had a greater permeability or incomplete recovery after challenges by LPS and thrombin. Histone deacetylase (HDAC) 6 deacetylates proteins essential for maintenance of endothelial barrier function. We found that HDAC6 phosphorylation at serine-22 was increased in lung tissues of mice exposed to CS and in lung ECs exposed to cigarette smoke extract (CSE). Inhibition of HDAC6 attenuated CSE-induced increases in EC permeability and CS priming of ALI. Similar barrier protection was provided by the microtubule stabilizer taxol, which preserved α-tubulin acetylation. CSE decreased α-tubulin acetylation and caused microtubule depolymerization. In coordination with increased HDAC6 phosphorylation, CSE inhibited Akt and activated glycogen synthase kinase (GSK)-3β; these effects were ameliorated by the antioxidant N-acetyl cysteine. Our results suggest that CS increases lung EC permeability, thereby enhancing susceptibility to ALI, likely through oxidative stress-induced Akt inactivation and subsequent GSK-3β activation. Activated GSK-3β may activate HDAC6 via phosphorylation of serine-22, leading to α-tubulin deacetylation and microtubule disassembly. Inhibition of HDAC6 may be a novel therapeutic option for ALI in cigarette smokers.
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