Cigarette Smoking Decreases Global MicroRNA Expression in Human Alveolar Macrophages

Graff, Joel W.; Powers, Linda S.; Dickson, Anne M.; Kim, Jong-Kwang; Reisetter, Anna C.; Hassan, Ihab; Kremens, Karol; Groß, Thomas; Wilson, Mary E.; Monick, Martha M.

doi:10.1371/journal.pone.0044066

Cited by 105 publications

(115 citation statements)

References 63 publications

(101 reference statements)

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“…The same phenomenon was also observed in alveolar macrophages of smokers, where (57). In this later study the decrease in global miRNA expression was more pronounced in heavy smokers, suggesting that the magnitude of miRNA repression is related to the extent of smoking history (57).…”

Section: Mirnas Repression By Cigarette Smoke In the Lungssupporting

confidence: 79%

“…These results are supported by the study of Schembri et al, who found that most of the differentially expressed miRNAs in the human bronchial airway epithelium were downregulated in smokers and were inversely correlated with their predicted targets (56). The same phenomenon was also observed in alveolar macrophages of smokers, where (57). In this later study the decrease in global miRNA expression was more pronounced in heavy smokers, suggesting that the magnitude of miRNA repression is related to the extent of smoking history (57).…”

Section: Mirnas Repression By Cigarette Smoke In the Lungssupporting

confidence: 74%

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A potential role for estrogen in cigarette smoke-induced microRNA alterations and lung cancer

Cohen

Burgos-Aceves²,

Smith³

2016

Transl. Lung Cancer Res.

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Alteration in the expression of microRNAs (miRNAs) is associated with oncogenesis and cancer progression. In this review we aim to suggest that elevated levels of estrogens and their metabolites inside the lungs as a result of cigarette smoke exposure can cause widespread repression of miRNA and contribute to lung tumor development. Anti-estrogenic compounds, such as the components of cruciferous vegetables, can attenuate this effect and potentially reduce the risk of lung cancer (LC) among smokers. (Table 1), and seem to work differently depending on the cellular context (47). However, developing any type of LC by deregulation of miRNAs via ER-Estrogen effect is still not entirely clear (8). miRNAs repression by cigarette smoke in the lungsWe have summarized before the results showing reduced expression levels of miRNAs in various tumors and cancer cell lines, including LC (48). The observation of a global miRNA repression in the lungs of rodents exposed to CS has also been reported (49)(50)(51)(52). Izzotti et al. show in their results the extensive down-regulation of 126 miRNAs in lungs of rats, 4 weeks after CS exposure (49). Such a short-lasting exposure to CS resulted in reversible miRNA alterations, as miRNA down-regulation was considerably attenuated one week after smoking cessation (51). By contrast, the repression of miRNA detected in mice exposed to CS for 4 months still persisted 3 months after smoking cessation, with the progressive development of cancer in the lung, suggesting that long-lasting exposure is needed to induce irreversible miRNA alterations (51,53). In their previous published results, using the same animal model, Izzotti et al. have found that CS up-regulates gene transcription and protein expression (54,55). The authors suggested that the CS-induced down-regulation of miRNA cause oncogene activation and cell proliferation, and that the persistence of these molecular alterations is crucial to commit lung cells towards carcinogenesis (51,53). These results are supported by the study of Schembri et al., who found that most of the differentially expressed miRNAs in the human bronchial airway epithelium were downregulated in smokers and were inversely correlated with their predicted targets (56). The same phenomenon was also observed in alveolar macrophages of smokers, where CS decreased global miRNA expression, while increased their predicted targets (57). In this later study the decrease in global miRNA expression was more pronounced in heavy smokers, suggesting that the magnitude of miRNA repression is related to the extent of smoking history (57). Anti-estrogenic compounds as attenuators of cigarette smoke effectsStudies suggest that phytochemicals from vegetables and fruits exhibit chemopreventive activities against various types of cancer (58). Izzotti et al. (59) evaluated miRNA expression in the lungs of rats exposed to CS and treated with several cancer chemopreventive agents. Administration of the dietary agents, Phenethyl isothiocyanate (PEITC) and Indole-3-carbi...

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Section: Mirnas Repression By Cigarette Smoke In the Lungssupporting

confidence: 79%

Section: Mirnas Repression By Cigarette Smoke In the Lungssupporting

confidence: 74%

A potential role for estrogen in cigarette smoke-induced microRNA alterations and lung cancer

Cohen

Burgos-Aceves²,

Smith³

2016

Transl. Lung Cancer Res.

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“…Exposure to cigarette smoke caused down-regulation of some miRNAs in mouse and rat lungs (Izzotti et al, 2009a(Izzotti et al, , 2009b, and the down-regulation in mouse lung was reversed by smoking cessation (Izzotti et al, 2011). Similar findings have been reported in humans; the levels of several miRNAs in airway epithelium (Schembri et al, 2009), placenta (Maccani et al, 2010, and alveolar macrophages (Graff et al, 2012) were lower in smokers than in non-smokers. These results lead us to speculate that miRNAs in tissues, including trachea and lung, exposed to cigarette smoke might leak into blood.…”

Section: Discussionsupporting

confidence: 64%

Cigarette smoking substantially alters plasma microRNA profiles in healthy subjects

Takahashi

Yokota

Tatsumi

et al. 2013

Toxicology and Applied Pharmacology

119

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Circulating microRNAs (miRNAs) are receiving attention as potential biomarkers of various diseases, including cancers, chronic obstructive pulmonary disease, and cardiovascular disease. However, it is unknown whether the levels of circulating miRNAs in a healthy subject might vary with external factors in daily life. In this study, we investigated whether cigarette smoking, a habit that has spread throughout the world and is a risk factor for various diseases, affects plasma miRNA profiles. We determined the profiles of 11 smokers and 7 non-smokers by TaqMan MicroRNA array analysis. A larger number of miRNAs were detected in smokers than in non-smokers, and the plasma levels of two thirds of the detected miRNAs (43 miRNAs) were significantly higher in smokers than in non-smokers. A principal component analysis of the plasma miRNA profiles clearly separated smokers and non-smokers. Twenty-four of the miRNAs were previously reported to be potential biomarkers of disease, suggesting the possibility that smoking status might interfere with the diagnosis of disease. Interestingly, we found that quitting smoking altered the plasma miRNA profiles to resemble those of non-smokers. These results suggested that the differences in the plasma miRNA profiles between smokers and non-smokers could be attributed to cigarette smoking. In addition, we found that an acute exposure of ex-smokers to cigarette smoke (smoking one cigarette) did not cause a dramatic change in the plasma miRNA profile. In conclusion, we found that repeated cigarette smoking substantially alters the plasma miRNA profile, interfering with the diagnosis of disease or signaling potential smoking-related diseases.

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“…To explore expression patterns at differentially methylated loci in the discovery cohort, we examined public data generated in airway and lung-related tissues available through the Gene Expression Omnibus (2,3,(20)(21)(22)(23)(24)(25)(26). Transcripts demonstrating nominally significant differences in expression (Student's t test P , 0.05) by current smoking status from selected studies are summarized in Table E8; at the majority of the loci examined, the direction of the expression changes were anticorrelated with the methylation changes observed in our analysis.…”

Section: Original Researchmentioning

confidence: 99%

Smoking-Associated Site-Specific Differential Methylation in Buccal Mucosa in the COPDGene Study

Wan

Qiu

Carey

et al. 2015

Am J Respir Cell Mol Biol

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DNA methylation is a complex, tissue-specific phenomenon that can reflect both endogenous factors and exogenous exposures. Buccal brushings represent an easily accessible source of DNA, which may be an appropriate surrogate tissue in the study of environmental exposures and chronic respiratory diseases. Buccal brushings were obtained from a subset of current and former smokers from the COPDGene study. Genome-wide DNA methylation data were obtained in the discovery cohort (n = 82) using the Illumina HumanMethylation450K array. Empirical Bayes methods were used to test for differential methylation by current smoking status at 468,219 autosomal CpG sites using linear models adjusted for age, sex, and race. Pyrosequencing was performed in a nonoverlapping replication cohort (n = 130). Current smokers were significantly younger than former smokers in both the discovery and replication cohorts. Seven CpG sites were associated with current smoking at a false discovery rate less than 0.05 in the discovery cohort. Six of the seven significant sites were pyrosequenced in the replication cohort; five CpG sites, including sites annotated to CYP1B1 and PARVA, were replicated. Correlations between cumulative smoke exposure and time since smoking cessation were observed in a subset of the significantly associated CpG sites. A significant correlation between reduced lung function and increased radiographic emphysema with methylation at cg02162897 (CYP1B1) was observed among female subjects. Site-specific methylation of DNA isolated from buccal mucosa is associated with exposure to cigarette smoke, and may provide insights into the mechanisms underlying differential susceptibility toward the development of smoking-related chronic respiratory diseases.

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Cigarette Smoking Decreases Global MicroRNA Expression in Human Alveolar Macrophages

Cited by 105 publications

References 63 publications

A potential role for estrogen in cigarette smoke-induced microRNA alterations and lung cancer

A potential role for estrogen in cigarette smoke-induced microRNA alterations and lung cancer

Cigarette smoking substantially alters plasma microRNA profiles in healthy subjects

Smoking-Associated Site-Specific Differential Methylation in Buccal Mucosa in the COPDGene Study

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