Genetic and epigenetic alterations in normal and sensitive COPD-diseased human bronchial epithelial cells repeatedly exposed to air pollution-derived PM 2.5

Leclercq, B.; Platel, Anne; Anthérieu, Sébastien; Alleman, L.; Hardy, EM; Perdrix, Espéranza; Grova, Nathalie; Riffault, Véronique; Appenzeller, Brice; Happillon, M.; Nesslany, Fabrice; Coddeville, P.; Lo-Guidice, Jean-Marc; Garçon, Guillaume

doi:10.1016/j.envpol.2017.06.028

Cited by 80 publications

(47 citation statements)

References 61 publications

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“…GWAS most frequently detects non-coding variants, and variants affecting gene expression have been shown to have pervasive effects on most diseases [46]. Histone markers like h3k9ac and h3k4me3 are some of the most essential modification markers involved in arterial pressure [47] and development of bronchial epithelial cells influencing COPD [48]. Super enhancer regions have multiple enhancers that drive transcription of genes involved in cell identity in diseases and heart development [49].…”

Section: Discussionmentioning

confidence: 99%

Genetic overlap of chronic obstructive pulmonary disease and cardiovascular disease-related traits: a large-scale genome-wide cross-trait analysis

Zhu

Wang

et al. 2019

Respir Res

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Background A growing number of studies clearly demonstrate a substantial association between chronic obstructive pulmonary disease (COPD) and cardiovascular diseases (CVD), although little is known about the shared genetics that contribute to this association. Methods We conducted a large-scale cross-trait genome-wide association study to investigate genetic overlap between COPD (N case = 12,550, N control = 46,368) from the International COPD Genetics Consortium and four primary cardiac traits: resting heart rate (RHR) ( N = 458,969), high blood pressure (HBP) (N case = 144,793, N control = 313,761), coronary artery disease (CAD)(N case = 60,801, N control = 123,504), and stroke (N case = 40,585, N control = 406,111) from UK Biobank, CARDIoGRAMplusC4D Consortium, and International Stroke Genetics Consortium data. Results RHR and HBP had modest genetic correlation, and CAD had borderline evidence with COPD at a genome-wide level. We found evidence of local genetic correlation with particular regions of the genome. Cross-trait meta-analysis of COPD identified 21 loci jointly associated with RHR, 22 loci with HBP, and 3 loci with CAD. Functional analysis revealed that shared genes were enriched in smoking-related pathways and in cardiovascular, nervous, and immune system tissues. An examination of smoking-related genetic variants identified SNPs located in 15q25.1 region associated with cigarettes per day, with effects on RHR and CAD. A Mendelian randomization analysis showed a significant positive causal effect of COPD on RHR (causal estimate = 0.1374, P = 0.008). Conclusion In a set of large-scale GWAS, we identify evidence of shared genetics between COPD and cardiac traits. Electronic supplementary material The online version of this article (10.1186/s12931-019-1036-8) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Genetic overlap of chronic obstructive pulmonary disease and cardiovascular disease-related traits: a large-scale genome-wide cross-trait analysis

Zhu

Wang

et al. 2019

Respir Res

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“…Tetra-OH-B[a]P and 8-OHdG levels are elevated in the DNA of primary human bronchial epithelial (HBE) cells from COPD patients compared to those in HBE from normal subjects. This indicates that COPD-DHBE cells were more sensitive to PM 2.5 derived from air pollution [ 62 ]. Transition metals in PM increase the levels of IL-8 and HO-1, leading to ROS production in mucus-secreting ALI-cultured primary bronchial epithelial cells (PBECs) [ 63 ].…”

Section: In Vitro Experimental Studies Of Pm 25 mentioning

confidence: 99%

In Vitro and In Vivo Experimental Studies of PM2.5 on Disease Progression

Cho

Hsieh

Tsai

et al. 2018

IJERPH

148

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Air pollution is a very critical issue worldwide, particularly in developing countries. Particulate matter (PM) is a type of air pollution that comprises a heterogeneous mixture of different particle sizes and chemical compositions. There are various sources of fine PM (PM2.5), and the components may also have different effects on people. The pathogenesis of PM2.5 in several diseases remains to be clarified. There is a long history of epidemiological research on PM2.5 in several diseases. Numerous studies show that PM2.5 can induce a variety of chronic diseases, such as respiratory system damage, cardiovascular dysfunction, and diabetes mellitus. However, the epidemiological evidence associated with potential mechanisms in the progression of diseases need to be proved precisely through in vitro and in vivo investigations. Suggested mechanisms of PM2.5 that lead to adverse effects and chronic diseases include increasing oxidative stress, inflammatory responses, and genotoxicity. The aim of this review is to provide a brief overview of in vitro and in vivo experimental studies of PM2.5 in the progression of various diseases from the last decade. The summarized research results could provide clear information about the mechanisms and progression of PM2.5-induced disease.

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“…In a comparable study exposing NHBE and COPD-DHBE cells with sampled PM2.5 air pollution from two different seasons (autumn-winter and spring-summer season) revealed shorter TLs and an increase in telomerase activity in a concentration-and exposuredependent manner. 77 A single exposure of 4 hours to 2 or 10 µg/cm 3 of PM2.5 did not alter TL and telomerase activity in both NHBD and COPD-DHBE cells compared with controls. However a three times repeated exposure of 4 hours to a concentration of 2 or 10 µg/cm 3 of PM2.5 significantly shortened TL and increased telomerase activity in NHBD and COPD-DHBE cells compared with controls.…”

Section: In Vitro and In Vivo Studies On Air Pollutant Exposures And mentioning

confidence: 78%

Ageing at the level of telomeres in association to residential landscape and air pollution at home and work: a review of the current evidence

Martens

Nawrot

2018

Toxicology Letters

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Studies suggest that leukocyte telomere length is an index of systemic ageing. Here, we discuss telomere length as a marker of biological ageing in relation to residential landscape (greenness), residential air pollution and work-related exposures. Telomere lengths are memories of cumulative oxidative and inflammatory stress, and show to have inverse associations with the risk of non-communicable diseases. For this reason, telomeres are considered as markers of biological ageing. Studies at birth, in children, young adulthood, and elderly show that residential green space, lower traffic exposure and long-term lower exposure to particulate air pollution are associated with longer telomeres. Work-related exposures including exposure to toxic metals, polycyclic aromatic hydrocarbons and particulate matter are associated with shorter telomeres for a given age. In contrast to chronic exposures, evidence is present of the observation that recent exposure is associated with longer telomeres. Our overview shows that the magnitude of residential and work-related environmental factors on telomere length are often as important as many classical lifestyle factors.

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Genetic and epigenetic alterations in normal and sensitive COPD-diseased human bronchial epithelial cells repeatedly exposed to air pollution-derived PM 2.5

Cited by 80 publications

References 61 publications

Genetic overlap of chronic obstructive pulmonary disease and cardiovascular disease-related traits: a large-scale genome-wide cross-trait analysis

Genetic overlap of chronic obstructive pulmonary disease and cardiovascular disease-related traits: a large-scale genome-wide cross-trait analysis

In Vitro and In Vivo Experimental Studies of PM2.5 on Disease Progression

Ageing at the level of telomeres in association to residential landscape and air pollution at home and work: a review of the current evidence

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