Role of epithelial mesenchymal transition (EMT) in chronic obstructive pulmonary disease (COPD)

Sohal, Sukhwinder Singh; Walters, E. Haydn

doi:10.1186/1465-9921-14-120

Cited by 53 publications

(44 citation statements)

References 18 publications

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“…EMT represents the loss of epithelial properties and the acquisition of mesenchymal cell characteristics, associated with pathological processes and tissue remodelling. EMT has previously been linked to COPD and cigarette smoke exposure [39,40]. The expression of miR-7 was also found to be altered by CSE.…”

Section: Introductionmentioning

confidence: 80%

Unravelling the complexity of COPD by microRNAs: it's a small world after all

et al. 2015

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Chronic obstructive pulmonary disease (COPD) is a progressive lung disease and is currently the fourth leading cause of death worldwide. Chronic inflammation and repair processes in the small airways are characteristic of COPD. Despite extensive efforts from researchers and industry, there is still no cure for COPD, hence an urgent need for new therapeutic alternatives. MicroRNAs are such an option; they are small noncoding RNAs involved in gene regulation. Their importance has been shown with respect to maintaining the balance between health and disease. Although previous reviews have discussed the expression of microRNAs related to lung disease, a detailed discussion regarding the function of differential miRNA expression in the pathogenesis of COPD is lacking.In this review we link the expression of microRNAs to different features of COPD and explain their importance in the pathogenesis of this disease. We further discuss their potential to contribute to the development of future therapeutic strategies. @ERSpublications Complexity of miRNAs in COPD: an up-to-date overview of the role of miRNAs in the different features of COPD http://ow.ly/Pk4FP

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Section: Introductionmentioning

confidence: 80%

Unravelling the complexity of COPD by microRNAs: it's a small world after all

et al. 2015

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“…In vitro studies using cigarette smoke condensate (CSC) on human bronchial epithelial cell lines show up-regulation of miR-101 and miR-144, which target the cystic fibrosis transmembrane conductance regulator found to mitigate airway cell inflammation, and also are found to be up-regulated in COPD (102, 103). Other changes in vitro include a decrease in miR-200c, related to NF-κB-mediated inflammation and thought to increase epithelial to mesenchymal transition (EMT) associated with tissue remodeling and cigarette smoking in COPD (104–107). Experimental animal models for cigarette smoke exposure have identified altered expression of several miRNAs including, miR-146a, miR-92a-2*, miR-147, miR-21 miR-20 and miR-181.…”

Section: Introductionmentioning

confidence: 99%

A Review of Pulmonary Toxicity of Electronic Cigarettes in the Context of Smoking: A Focus on Inflammation

Shields

Berman

Brasky

et al. 2017

Cancer Epidemiology, Biomarkers &Amp; Prevention

107

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The use of electronic cigarettes (e-cigs) is increasing rapidly, but their effects on lung toxicity are largely unknown. Smoking is a well-established cause of lung cancer and respiratory disease, in part through inflammation. It is plausible that e-cig use might affect similar inflammatory pathways. E-cigs are used by some smokers as an aid for quitting or smoking reduction, and by never smokers (e.g., adolescents and young adults). The relative effects for impacting disease risk may differ for these groups. Cell culture and experimental animal data indicate that e-cigs have the potential for inducing inflammation, albeit much less than smoking. Human studies show that e-cig use in smokers is associated with substantial reductions in blood or urinary biomarkers of tobacco toxicants when completely switching and somewhat for dual use. However, the extent to which these biomarkers are surrogates for potential lung toxicity remains unclear. The FDA now has regulatory authority over e-cigs and can regulate product and e-liquid design features such as nicotine content and delivery, voltage, e-liquid formulations, and flavors. All of these factors may impact pulmonary toxicity. This review summarizes current data on pulmonary inflammation related to both smoking and e-cig use, with a focus on human lung biomarkers.

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“…[51] The increasing amounts of evidence for EMT in pathology of IPF and COPD are documented. [52] Notably, the mechanism of EMT in COPD are thought to be initiated with breakdown of basement membrane containing fibronectin, resulting in stimulation of epithelial cell migration with mesenchymal cell transition [53] in combination with the increased vessel-associated TGF-β in lung tissues of smokers and COPD patients. [54] The isoAsp residue formation in ECM proteins might participate in one of the mechanism of EMT in COPD lung.…”

Section: Discussionmentioning

confidence: 99%