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

Osei, Emmanuel T.; Florez-Sampedro, Laura; Timens, Wim; Postma, Dirkje S.; Heijink, Irene H.; Brandsma, Corry‐Anke

doi:10.1183/13993003.02139-2014

Cited by 77 publications

(65 citation statements)

References 69 publications

(108 reference statements)

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“…In vitro and in vivo studies have shown that miRNAs play a crucial role in cellular response to stress as well as cell growth and death 35, 36, 49, 50 . The airway epithelial miRNA transcriptome changes in response to cigarette smoke exposure 35, 49 , and miRNAs have been implicated in COPD pathology 35, 49, 51 .…”

Section: Discussionmentioning

confidence: 99%

“…The airway epithelial miRNA transcriptome changes in response to cigarette smoke exposure 35, 49 , and miRNAs have been implicated in COPD pathology 35, 49, 51 . A main goal of this study was to determine the global effects of eCig exposure upon miRNA expression, and test whether miRNAs alter expression of their target mRNA in eCig-exposed lung epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA expression profiling defines the impact of electronic cigarettes on human airway epithelial cells

Solleti

Bhattacharya

Aḥmad

et al. 2017

Sci Rep

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While all forms of tobacco exposure have negative health effects, the significance of exposure to electronic cigarettes (eCig) is not fully understood. Here, we studied the global effects of eCig on the micro RNA (miRNA) transcriptome in human lung epithelial cells. Primary human bronchial epithelial (NHBE) cells differentiated at air-liquid interface were exposed to eCig liquid. Exposure of NHBE to any eCig liquid resulted in the induction of oxidative stress-response genes including GCLM, GCLC, GPX2, NQO1 and HO-1. Vaporization of, and/or the presence of nicotine in, eCig liquid was associated with a greater response. We identified 578 miRNAs dysregulated by eCig exposure in NHBE, and 125 miRNA affected by vaporization of eCig liquid. Nicotine containing eCig vapor displayed the most profound effects upon miRNA expression. We selected 8 miRNAs (29A, 140, 126, 374A, 26A-2, 147B, 941 and 589) for further study. We validated increased expression of multiple miRNAs, including miR126, following eCig exposure. We also found significant reduction in the expression of two miR126 target genes, MYC and MRGPRX3, following exposure. These data demonstrated that eCig exposure has profound effects upon gene expression in human lung epithelial cells, some of which are epigenetically programmed at the level of miRNA regulation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MicroRNA expression profiling defines the impact of electronic cigarettes on human airway epithelial cells

Solleti

Bhattacharya

Aḥmad

et al. 2017

Sci Rep

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show abstract

“…The major function of both the up- and down-regulated miRNAs was inflammation, with several targets associated with NF-κB pathway. There are other examples of miRNAs related to cigarette smoke and inflammation considered to be involved in COPD, such as effects in smooth muscle, fibroblasts, macrophages and neutrophils, and specific miRNA changes in bronchial epithelia of smokers versus non-smokers (97, 116). …”

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

110

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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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“…BAKER et al [94] postulate that the reduced expression of both Sirtuins is regulated by the microRNA MiR-34a, a small endogenous noncoding RNA, which appears to be increased in COPD patients compared to controls. Although the role of microRNAs in COPD has been extensively reviewed [96] the role of microRNAs in accelerated lung ageing is not extensively investigated and remains rather elusive [97].…”

Section: Epigenetic Changesmentioning

confidence: 99%

Lung ageing and COPD: is there a role for ageing in abnormal tissue repair?

et al. 2017

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Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide, with increasing prevalence, in particular in the elderly. COPD is characterised by abnormal tissue repair resulting in (small) airways disease and emphysema. There is accumulating evidence that ageing hallmarks are prominent features of COPD. These ageing hallmarks have been described in different subsets of COPD patients, in different lung compartments and also in a variety of cell types, and thus might contribute to different COPD phenotypes. A better understanding of the main differences and similarities between normal lung ageing and the pathology of COPD may improve our understanding of the mechanisms driving COPD pathology, in particular in those patients that develop the most severe form of COPD at a relatively young age, i.e. severe early-onset COPD patients.In this review, after introducing the main concepts of lung ageing and COPD pathology, we focus on the role of (abnormal) ageing in lung remodelling and repair in COPD. We discuss the current evidence for the involvement of ageing hallmarks in these pathological features of COPD. We also highlight potential novel treatment strategies and opportunities for future research based on our current knowledge of abnormal lung ageing in COPD.

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

Cited by 77 publications

References 69 publications

MicroRNA expression profiling defines the impact of electronic cigarettes on human airway epithelial cells

MicroRNA expression profiling defines the impact of electronic cigarettes on human airway epithelial cells

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

Lung ageing and COPD: is there a role for ageing in abnormal tissue repair?

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