Exposure of airway epithelial cells to cigarette smoke extract causes the release of extracellular vesicles via thiol-reactive carbonyl compounds

Pneumologie ◽  
2016 ◽  
Vol 70 (S 01) ◽  
Author(s):  
B Benedikter ◽  
C Volgers ◽  
EFM Wouters ◽  
PHM Savelkoul ◽  
GRMM Haenen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Extracellular Vesicles ◽  
Carbonyl Compounds ◽  
Cigarette Smoke Extract ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Reactive Carbonyl Compounds ◽  
Reactive Carbonyl

scholarly journals Cigarette Smoke Condensate Exposure Changes RNA Content of Extracellular Vesicles Released from Small Airway Epithelial Cells

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1652
Author(s):  
Tiziana Corsello ◽  
Andrzej S. Kudlicki ◽  
Roberto P. Garofalo ◽  
Antonella Casola
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Extracellular Vesicles ◽  
Viral Infections ◽  
Cell Communication ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Cigarette Smoke Condensate ◽  
Diverse Range ◽  
Chronic Lung Diseases

Exposure to environmental tobacco smoke (ETS) is a known risk factor for the development of chronic lung diseases, cancer, and the exacerbation of viral infections. Extracellular vesicles (EVs) have been identified as novel mediators of cell–cell communication through the release of biological content. Few studies have investigated the composition/function of EVs derived from human airway epithelial cells (AECs) exposed to cigarette smoke condensate (CSC), as surrogates for ETS. Using novel high-throughput technologies, we identified a diverse range of small noncoding RNAs (sncRNAs), including microRNA (miRNAs), Piwi-interacting RNA (piRNAs), and transfer RNA (tRNAs) in EVs from control and CSC-treated SAE cells. CSC treatment resulted in significant changes in the EV content of miRNAs. A total of 289 miRNAs were identified, with five being significantly upregulated and three downregulated in CSC EVs. A total of 62 piRNAs were also detected in our EV preparations, with five significantly downregulated and two upregulated in CSC EVs. We used TargetScan and Gene Ontology (GO) analysis to predict the biological targets of hsa-miR-3913-5p, the most represented miRNA in CSC EVs. Understanding fingerprint molecules in EVs will increase our knowledge of the relationship between ETS exposure and lung disease, and might identify potential molecular targets for future treatments.

scholarly journals A Protective Role of FAM13A in Human Airway Epithelial Cells Upon Exposure to Cigarette Smoke Extract

2021 ◽  
Vol 12 ◽  
Author(s):  
Qing Chen ◽  
Maaike de Vries ◽  
Kingsley Okechukwu Nwozor ◽  
Jacobien A. Noordhoek ◽  
Corry-Anke Brandsma ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoking ◽  
Cigarette Smoke ◽  
Airway Epithelium ◽  
Barrier Function ◽  
Cigarette Smoke Extract ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Copd Patients ◽  
Epithelial Resistance

BackgroundChronic Obstructive Pulmonary Disease (COPD) is a progressive lung disease characterized by chronic inflammation upon inhalation of noxious particles, e.g., cigarette smoke. FAM13A is one of the genes often found to be associated with COPD, however its function in the pathophysiology of COPD is incompletely understood. We studied its role in airway epithelial barrier integrity and cigarette smoke-induced epithelial responses.Materials and MethodsProtein level and localization of FAM13A was assessed with immunohistochemistry in lung tissue from COPD patients and non-COPD controls. In vitro, FAM13A expression was determined in the absence or presence of cigarette smoke extract (CSE) in primary airway epithelial cells (AECs) from COPD patients and controls by western blotting. FAM13A was overexpressed in cell line 16HBE14o- and its effect on barrier function was monitored real-time by electrical resistance. Expression of junctional protein E-cadherin and β-catenin was assessed by western blotting. The secretion of neutrophil attractant CXCL8 upon CSE exposure was measured by ELISA.ResultsFAM13A was strongly expressed in airway epithelium, but significantly weaker in airways of COPD patients compared to non-COPD controls. In COPD-derived AECs, but not those of controls, FAM13A was significantly downregulated by CSE. 16HBE14o- cells overexpressing FAM13A built up epithelial resistance significantly more rapidly, which was accompanied by higher E-cadherin expression and reduced CSE-induced CXCL8 levels.ConclusionOur data indicate that the expression of FAM13A is lower in airway epithelium of COPD patients compared to non-COPD controls. In addition, cigarette smoking selectively downregulates airway epithelial expression of FAM13A in COPD patients. This may have important consequences for the pathophysiology of COPD, as the more rapid build-up of epithelial resistance upon FAM13A overexpression suggests improved (re)constitution of barrier function. The reduced epithelial secretion of CXCL8 upon CSE-induced damage suggests that lower FAM13A expression upon cigarette smoking may facilitate epithelial-driven neutrophilia.

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