Abstract
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.
Highlights
Environmental tobacco smoke (ETS) exposure is associated with an increased frequency of lower respiratory tract infections, increased incidence and severity of asthma episodes, overall decreased pulmonary function, and cancer development.Extracellular vesicles (EVs) are membrane particles released by virtually all cells, shuttling active biological molecules such as proteins, lipids, and nucleic acids to neighboring cells, and to distant sites [1,2,3]
small airway epithelial (SAE) cells of the control group produced an average of 9.2 × 107 particles/mL, and SAE cells in the cigarette smoke condensate (CSC)-treated group produced an average of 8.0 × 107 particles/mL (Figure 2A), indicating a similar particle release between control and treated cells
Recent in vitro study reported that human bronchial epithelial (HBE) cells exposed to cigarette smoke extract (CSE) released EVs, and EVs from both normal and CSE-treated cell conditions displayed the expression of CD63, the EV
Summary
Environmental tobacco smoke (ETS) exposure is associated with an increased frequency of lower respiratory tract infections, increased incidence and severity of asthma episodes, overall decreased pulmonary function, and cancer development.Extracellular vesicles (EVs) are membrane particles released by virtually all cells, shuttling active biological molecules such as proteins, lipids, and nucleic acids to neighboring cells, and to distant sites [1,2,3]. EVs represent a heterogeneous population and vary in size (30–2000 nm in diameter) and composition, based on the cellular origin and environmental stimuli [10,11,12]. According to their diameter, EVs can be classified into two general subgroups: 1) small. Recent studies have identified EVs as critical players in intercellular communication under various physiological and pathological conditions such as neurodegenerative diseases, cancer, preterm birth, angiogenesis, immune responses, and viral infections [3,13,14,15,16,17,18,19,20]
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