Bronchial epithelial cell extracellular vesicles ameliorate epithelial–mesenchymal transition in COPD pathogenesis by alleviating M2 macrophage polarization

He, Sheng Yang; Chen, Duanni; Hu, Mengyun; Zhang, Li; Liu, Caihong; Traini, Daniela; Grau, Georges E.; Zeng, Zhengpeng; Lu, Junjuan; Zhou, Guanzhi; Xie, Li; Sun, Shenghua

doi:10.1016/j.nano.2019.03.010

Cited by 55 publications

(53 citation statements)

References 52 publications

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“…Recent studies demonstrated that two miRNAs, miR-210 and miR-21, were upregulated in EVs after cell exposure to CSE [25,47]. When using BEAS 2B cells, He and colleagues found that a low percentage of CSE reduced the amount of miR-21 while a higher CSE percentage increased the miR-21 content of EVs [48]. In our experiments, miR-21 was detectable in both CSC and control EVs, with a marginal increase in the CSC ones, which, however, was not statistically significant.…”

Section: Discussionmentioning

confidence: 99%

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

Corsello

Kudlicki

Garofalo

et al. 2019

Cells

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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.

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Section: Discussionmentioning

confidence: 99%

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

Corsello

Kudlicki

Garofalo

et al. 2019

Cells

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“…Furthermore, the levels of exosomal miR-21 were high in sera of smokers and COPD patients and are inversely correlated with Forced Expiratory Volume in one second/Forced Vital Capacity (FEV1/FVC), which highlights the potential value of exosomal mir-21 for diagnosis and treatment of COPD. Recently, He et al have demonstrated that bronchial ECs could generate EVs with less miR-21 when treated with CS extract, alleviating the polarization of M2 macrophages, which indirectly modulate the EMT process in the COPD pathogenesis [41]. Previously, Fujita et al also observed that CS induced relative upregulation of miR-210 expression in both bronchial ECs and their corresponding EVs [31].…”

Section: Impact Of Exosomal Micrornas In Lung Diseasesmentioning

confidence: 99%

Exosomal miRNAs in Lung Diseases: From Biologic Function to Therapeutic Targets

Guiot

Struman

Louis

et al. 2019

JCM

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Increasing evidence suggests the potential role of extracellular vesicles (EVs) in many lung diseases. According to their subcellular origin, secretion mechanism, and size, EVs are currently classified into three subpopulations: exosomes, microvesicles, and apoptotic bodies. Exosomes are released in most biofluids, including airway fluids, and play a key role in intercellular communication via the delivery of their cargo (e.g., microRNAs (miRNAs)) to target cell. In a physiological context, lung exosomes present protective effects against stress signals which allow them to participate in the maintenance of lung homeostasis. The presence of air pollution alters the composition of lung exosomes (dysregulation of exosomal miRNAs) and their homeostatic property. Indeed, besides their potential as diagnostic biomarkers for lung diseases, lung exosomes are functional units capable of dysregulating numerous pathophysiological processes (including inflammation or fibrosis), resulting in the promotion of lung disease progression. Here, we review recent studies on the known and potential role of lung exosomes/exosomal miRNAs, in the maintaining of lung homeostasis on one hand, and in promoting lung disease progression on the other. We will also discuss using exosomes as prognostic/diagnostic biomarkers as well as therapeutic tools for lung diseases.

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“…Epithelial-mesenchymal transition (EMT) in bronchial epithelial cells is involved in pathogenesis of lung cancer, chronic obstructive pulmonary disease (COPD), asthma and pulmonary fibrosis, which all have a high prevalence [1][2][3][4]. IL-17A is involved in these lung diseases.…”

Section: Introductionmentioning

confidence: 99%

Cigarette and IL-17A synergistically induce bronchial epithelial-mesenchymal transition via activating IL-17R/NF-κB signaling

Jiang

Zhao

et al. 2020

BMC Pulm Med

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Background: IL-17A directly induces epithelial-mesenchymal transition (EMT) in alveolar epithelial cells. It could coordinate with cigarette smoke extract (CSE) to promote proliferation of bronchial epithelial cells. In this study, we aim to explore the direct effect of IL-17A and CSE on EMT in bronchial epithelial cells. Methods: Bronchial epithelial cells were isolated from C57BL/6 mice, and cocultured with CSE or/and IL-17A. Ecadherin and Vimentin expressions in cells were detected using immunofluorescence staining. IL-17R expression was detected using immunohistochemistry staining. NF-κB expression was assessed using western blotting. When NF-κB was inhibited by BAY 11-7821, expressions of NF-κB, E-cadherin and Vimentin were measured. Results: The protein expression of E-cadherin in bronchial epithelial cells was lowest in CSE + IL-17A group, followed by CSE group. In contrast, the protein expression of Vimentin was highest in CSE + IL-17A group, followed by CSE group. Similarly, IL-17R and NF-κB expressions were highest in CSE + IL-17A group, followed by CSE group and IL-17A group. NF-κB inhibitor could inhibit the expressions of E-cadherin and Vimentin. Conclusions: Cigarette and IL-17A could synergistically induce EMT in bronchial epithelial cells through activating IL17R/NF-κB signaling. Our findings contribute to a better understanding in airway EMT and pathogenesis of respiratory diseases, which are involved IL-17A and cigarette smoking. Those will provide novel avenues in the immunotherapy of lung diseases.

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Bronchial epithelial cell extracellular vesicles ameliorate epithelial–mesenchymal transition in COPD pathogenesis by alleviating M2 macrophage polarization

Cited by 55 publications

References 52 publications

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

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

Exosomal miRNAs in Lung Diseases: From Biologic Function to Therapeutic Targets

Cigarette and IL-17A synergistically induce bronchial epithelial-mesenchymal transition via activating IL-17R/NF-κB signaling

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