In vitro evaluation of organic extractable matter from ambient PM2.5 using human bronchial epithelial BEAS-2B cells: Cytotoxicity, oxidative stress, pro-inflammatory response, genotoxicity, and cell cycle deregulation

Abbas, Imane; Badran, Ghidaa; Verdin, Anthony; Ledoux, Frédéric; Roumié, M.; Guidice, Jean‐Marc Lo; Courcot, Dominique; Garçon, Guillaume

doi:10.1016/j.envres.2019.01.052

Cited by 85 publications

(28 citation statements)

References 67 publications

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“…We conclude that (1) the most sensitive events for assessment of exposure to low PM0.5 concentration are the activation of AhR-and p53-dependent pathways together with GREM1, EGR1 and GDF15 induction and that (2) chemical components adhered to the surface of nanoparticles (such as polycyclic aromatic hydrocarbons and other AhR agonists) are responsible for the observed adverse effects. This hypothesis has been already suggested previously [8,54] and is supported by studies on the effects of extractable organic matter from PM [57][58][59].…”

Section: Discussionsupporting

confidence: 74%

Screening of Cellular Stress Responses Induced by Ambient Aerosol Ultrafine Particle Fraction PM0.5 in A549 Cells

Šimečková¹,

Marvanová²,

Kulich³

et al. 2019

IJMS

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Effects of airborne particles on the expression status of markers of cellular toxic stress and on the release of eicosanoids, linked with inflammation and oxidative damage, remain poorly characterized. Therefore, we proposed a set of various methodological approaches in order to address complexity of PM0.5-induced toxicity. For this purpose, we used a well-characterized model of A549 pulmonary epithelial cells exposed to a non-cytotoxic concentration of ambient aerosol particle fraction PM0.5 for 24 h. Electron microscopy confirmed accumulation of PM0.5 within A549 cells, yet, autophagy was not induced. Expression profiles of various cellular stress response genes that have been previously shown to be involved in early stress responses, namely unfolded protein response, DNA damage response, and in aryl hydrocarbon receptor (AhR) and p53 signaling, were analyzed. This analysis revealed induction of GREM1, EGR1, CYP1A1, CDK1A, PUMA, NOXA and GDF15 and suppression of SOX9 in response to PM0.5 exposure. Analysis of eicosanoids showed no oxidative damage and only a weak anti-inflammatory response. In conclusion, this study helps to identify novel gene markers, GREM1, EGR1, GDF15 and SOX9, that may represent a valuable tool for routine testing of PM0.5-induced in vitro toxicity in lung epithelial cells.

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Section: Discussionsupporting

confidence: 74%

Screening of Cellular Stress Responses Induced by Ambient Aerosol Ultrafine Particle Fraction PM0.5 in A549 Cells

Šimečková¹,

Marvanová²,

Kulich³

et al. 2019

IJMS

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“…NIA showed preventive action against protein oxidation induced by PM 2.5 . Previous study noted that PM 2.5 caused early arrest of cell cycle, resulting from induced DNA damage, and 8-oxoG, the oxidative stress biomarker, is the predominant adduct of ROS-induced oxidative changes (Abbas et al ., 2019). NIA has been shown to improve DNA repair following damage induced by ultraviolet radiation (Park et al ., 2010; Snaidr et al ., 2019).…”

Section: Discussionmentioning

confidence: 99%

Niacinamide Protects Skin Cells from Oxidative Stress Induced by Particulate Matter

Zhen

Piao

Kang

et al. 2019

Biomolecules & Therapeutics

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Niacinamide (NIA) is a water-soluble vitamin that is widely used in the treatment of skin diseases. Moreover, NIA displays antioxidant effects and helps repair damaged DNA. Recent studies showed that particulate matter 2.5 (PM2.5) induced reactive oxygen species (ROS), causing disruption of DNA, lipids, and protein, mitochondrial depolarization, and apoptosis of skin keratinocytes. Here, we investigated the protective effects of NIA on PM2.5-induced oxidative stress in human HaCaT keratinocytes. We found that NIA could inhibit the ROS generation induced by PM2.5, as well block the PM2.5-induced oxidation of molecules, such as lipids, proteins, and DNA. Furthermore, NIA alleviated PM2.5-induced accumulation of cellular Ca2+, which caused cell membrane depolarization and apoptosis, and reduced the number of apoptotic cells. Collectively, the findings show that NIA can protect keratinocytes from PM2.5-induced oxidative stress and cell damage.

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“…In vitro experiments consistently demonstrated that PM 2.5 can affect cell viability, inflammation response and intracellular ROS in a time-dependent manner [55,60]. However, we found that there were no significant difference in system inflammation, lung injury, pulmonary GSH/GSSH ratio, 3′-NT and 4-HNE levels and antioxidant enzymes (PRDX4, PRDX5, SOD1, SOD2, SOD3 and TRXR2) expression between PM 2.5 –3L and PM 2.5 –6L groups, indicating that exposure time had no obvious effect on PM 2.5 -induced inflammation and oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

The effect of exposure time and concentration of airborne PM2.5 on lung injury in mice: A transcriptome analysis

et al. 2019

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The association between airborne fine particulate matter (PM 2.5 ) concentration and the risk of respiratory diseases has been well documented by epidemiological studies. However, the mechanism underlying the harmful effect of PM 2.5 has not been fully understood. In this study, we exposed the C57BL/6J mice to airborne PM 2.5 for 3 months (mean daily concentration ~50 or ~110 μg/m 3 , defined as PM 2.5 –3L or PM 2.5 –3H) or 6 months (mean daily concentration ~50 μg/m 3 , defined as PM 2.5 –6L) through a whole-body exposure system. Histological and biochemical analysis revealed that PM 2.5 –3H exposure caused more severe lung injury than did PM 2.5 –3L, and the difference was greater than that of PM 2.5 –6L vs PM 2.5 –3L exposure. With RNA-sequencing technique, we found that the lungs exposed with different concentration of PM 2.5 have distinct transcriptional profiles. PM 2.5 –3H exposure caused more differentially expressed genes (DEGs) in lungs than did PM 2.5 –3L or PM 2.5 –6L. The DEGs induced by PM 2.5 –3L or PM 2.5 –6L exposure were mainly enriched in immune pathways, including Hematopoietic cell lineage and Cytokine-cytokine receptor interaction, while the DEGs induced by PM 2.5 –3H exposure were mainly enriched in cardiovascular disease pathways, including Hypertrophic cardiomyopathy and Dilated cardiomyopathy. In addition, we found that upregulation of Cd5l and reduction of Hspa1 and peroxiredoxin-4 was associated with PM 2.5 -induced pulmonary inflammation and oxidative stress. These results may provide new insight into the cytotoxicity mechanism of PM 2.5 and help to development of new strategies to attenuate air pollution associated respiratory disease.

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In vitro evaluation of organic extractable matter from ambient PM2.5 using human bronchial epithelial BEAS-2B cells: Cytotoxicity, oxidative stress, pro-inflammatory response, genotoxicity, and cell cycle deregulation

Cited by 85 publications

References 67 publications

Screening of Cellular Stress Responses Induced by Ambient Aerosol Ultrafine Particle Fraction PM0.5 in A549 Cells

Screening of Cellular Stress Responses Induced by Ambient Aerosol Ultrafine Particle Fraction PM0.5 in A549 Cells

Niacinamide Protects Skin Cells from Oxidative Stress Induced by Particulate Matter

The effect of exposure time and concentration of airborne PM2.5 on lung injury in mice: A transcriptome analysis

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