ArticleRespiratory research2013
Pyocyanin-induced mucin production is associated with redox modification of FOXA2.
Article in Respiratory research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 41 citations in OpenAlex.
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- Differential Metabolite Production Underlies Disruption of the Cystic Fibrosis Airway Microbiota by Pathogens.bioRxiv : the preprint server for biology · 2026Article
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- Semaglutide and pioglitazone restore airway mucosal homeostasis by resolvingFrontiers in immunology · 2026Article
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- Modulation of pulmonary immune functions by theFrontiers in immunology · 2025Review
- Ubiquitin-specific protease-7 promotes expression of airway mucin MUC5AC via the NF-κB signaling pathway.Heliyon · 2024Article
- FOXA2 Suppression by TRIM36 Exerts Anti-Tumor Role in Colorectal Cancer Via Inducing NRF2/GPX4-Regulated Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Infection, Allergy, and Inflammation: The Role ofMicroorganisms · 2023Review
- 7-Ethoxycoumarin rescued Caenorhabditis elegans from infection of COPD derived clinical isolate Pseudomonas aeruginosa through virulence and biofilm inhibition via targeting Rhl and Pqs quorum sensing systems.World journal of microbiology & biotechnology · 2023Article
- The COPD-Associated Polymorphism Impairs the CFTR Function to Suppress Excessive IL-8 Production upon Environmental Pathogen Exposure.International journal of molecular sciences · 2023Article
- A Maverick Review of Common Stem/Progenitor Markers in Lung Development.Stem cell reviews and reports · 2022Review
- The anti-inflammatory feature of glucagon-like peptide-1 and its based diabetes drugs-Therapeutic potential exploration in lung injury.Acta pharmaceutica Sinica. B · 2022Review
- Respiratory MUC5B disproportion is involved in severe community-acquired pneumonia.BMC pulmonary medicine · 2022Article
- An Organ System-Based Synopsis ofVirulence · 2021Review
- Random Peptide Mixtures as Safe and Effective Antimicrobials againstACS infectious diseases · 2021Article
- Dynamic Behavior of Aluminum Alloy Aw 5005 Undergoing Interfacial Friction and Specimen Configuration in Split Hopkinson Pressure Bar System at High Strain Rates and Temperatures.Materials (Basel, Switzerland) · 2020Article
- MUC1 contributes to goblet cell metaplasia and MUC5AC expression in response to cigarette smoke in vivo.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Exendin-4 restores airway mucus homeostasis through the GLP1R-PKA-PPARγ-FOXA2-phosphatase signaling.Mucosal immunology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe redox-active pyocyanin (PCN) is a toxic, secondary metabolite secreted by the respiratory pathogen Pseudomonas aeruginosa (PA). Previously, we have shown that mouse lungs chronically exposed to PCN develop goblet cell hyperplasia and metaplasia (GCHM) and mucus hypersecretion, fibrosis and emphysema. These pathological features are commonly found in the airways of several chronic lung diseases, including cystic fibrosis (CF), as well as in mouse airways deficient in the forkhead box A2 (FOXA2), a transcriptional repressor of goblet GCHM and mucus biosynthesis. Furthermore, PCN inhibits FOXA2 by activating the pro-GCHM signaling pathways Stat6 and EGFR. However, it is not known whether PCN-generated reactive oxygen (ROS) and nitrogen (RNS) species posttranslationally modify and inactivate FOXA2.
methodsWe examined the posttranslational modifications of FOXA2 by PCN using specific antibodies against oxidation, nitrosylation, acetylation and ubiquitination. Electrophoretic mobility shift assay (EMSA) was used to examine the ability of modified FOXA2 to bind the promoter of MUC5B mucin gene. In addition, we used quantitative real time PCR, ELISA, immunofluorescence and mouse lung infection to assess whether the loss of FOXA2 function caused GCHM and mucin overexpression. Finally, we examined the restoration of FOXA2 function by the antioxidant glutathione (GSH).
resultsWe found that PCN-generated ROS/RNS caused nitrosylation, acetylation, ubiquitination and degradation of FOXA2. Modified FOXA2 had reduced ability to bind the promoter of the MUC5B gene. The antioxidant GSH alleviated the modification of FOXA2 by PCN, and inhibited the overexpression of MUC5AC and MUC5B mucins.
conclusionThese results suggest that PCN-mediated posttranslational modifications of FOXA2 are positively correlated with GCHM and overexpression of airway mucins. Furthermore, antioxidant treatment restores the function of FOXA2 to attenuate GCHM and mucus hypersecretion.
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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.