Short- and Long- Term Effects of Cigarette Smoke Exposure on Glutathione Homeostasis in Human Bronchial Epithelial Cells

Bazzini, Claudia; Rossetti, V.; Civello, Davide Antonio; Sassone, Francesca; Vezzoli, Valeria; Persani, Luca; Tiberio, Laura; Lanata, Luigi; Bagnasco, Michela; Paulmichl, Markus; Meyer, Gerd; Garavaglia, Maria Lisa

doi:10.1159/000356633

Cited by 44 publications

(38 citation statements)

References 62 publications

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“…DCF fluorescence was used to measure ROS in cells exposed to CSE, in the absence or presence of 14,15-EET. In line with published data [27,28], CSE significantly increased ROS generation in Beas-2B cells 6 hrs after CSE exposure (Fig. 5).…”

Section: 15-eet Attenuate Ros Generation In Beas-2bsupporting

confidence: 92%

14,15-Epoxyeicosatrienoic Acid Suppresses Cigarette Smoke Extract-Induced Apoptosis in Lung Epithelial Cells by Inhibiting Endoplasmic Reticulum Stress

Zhang

Wang

et al. 2015

Cell Physiol Biochem

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Background/Aims: Epoxyeicosatrienoic acids (EETs), a type of lipid mediators produced by cytochrome P450 epoxygenases, exert anti-inflammatory, angiogenic, anti-oxidative and anti-apoptotic effects. However, the role of EETs in cigarette smoke-induced lung injury and the underlying mechanisms are not fully known. The aim of this study was to explore the effects of CYP2J2-EETs on cigarette smoke extracts (CSE)-induced apoptosis in human bronchial epithelial cell line (Beas-2B) and the possible mechanisms involved. Methods: Cytochrome P450 epoxygenase 2J2 (CYP2J2) and its metabolites EETs were assessed by western blotting or LC-MS-MS. Cell viability and apoptosis were determined by MTT assay and AnnexinV-PI staining. Reactive oxygen species (ROS) were assessed by measuring H2DCFDA. Caspase-3, HO-1, MAPK and endoplasmic reticulum (ER) stress-related markers GRP78, p-elF2a, and CHOP were evaluated by western blotting. Results: CSE suppressed expression of both CYP2J2 and EET by Beas-2B cells. CSE also induced apoptosis, the generation of ROS and the ER stress in Beas-2B cells. These changes were abolished by pretreatment with exogenous 14,15-EET while pretreatment with 14,15-EEZE, a selective EET antagonist, abolished the protective effects of 14,15-EET. In addition, EETs increased the expression of antioxidant enzyme HO-1. Furthermore, 14,15-EET reduced CSE-induced activation of p38 and JNK. Conclusion: The data suggest that CYP2J2-derived EETs protect against CSE-induced lung injury possibly through attenuating ER stress.

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Section: 15-eet Attenuate Ros Generation In Beas-2bsupporting

confidence: 92%

14,15-Epoxyeicosatrienoic Acid Suppresses Cigarette Smoke Extract-Induced Apoptosis in Lung Epithelial Cells by Inhibiting Endoplasmic Reticulum Stress

Zhang

Wang

et al. 2015

Cell Physiol Biochem

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“…It is interesting that many of the altered proteins were involved in key pathways that would be used to ameliorate the increased toxic burden, including proteins involved in the detoxification of xenobiotics, e.g. aldehyde dehydrogenase (ALDH3A1)31 or carbonyl reductase (CBR1)32 and proteins like peroxiredoxin (PRDX2) and glutathione reductase (GSR)33 that are required to metabolize reactive oxygen species. Reactive oxygen species are thought to contribute to the toxicity of tobacco exposure34 and upregulation of these proteins is likely a contributory response to this process.…”

Section: Discussionmentioning

confidence: 99%

Little Cigars are More Toxic than Cigarettes and Uniquely Change the Airway Gene and Protein Expression

Ghosh

Abdelwahab

Reeber

et al. 2017

Sci Rep

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Little cigars (LCs) are regulated differently than cigarettes, allowing them to be potentially targeted at youth/young adults. We exposed human bronchial epithelial cultures (HBECs) to air or whole tobacco smoke from cigarettes vs. LCs. Chronic smoke exposure increased the number of dead cells, lactate dehydrogenase release, and interleukin-8 (IL-8) secretion and decreased apical cilia, cystic fibrosis transmembrane conductance regulator (CFTR) protein levels, and transepithelial resistance. These adverse effects were significantly greater in LC-exposed HBECs than cigarette exposed cultures. LC-exposure also elicited unique gene expression changes and altered the proteomic profiles of airway apical secretions compared to cigarette-exposed HBECs. Gas chromatography-mass spectrometry (GC-MS) analysis indicated that LCs produced more chemicals than cigarettes, suggesting that the increased chemical load of LCs may be the cause of the greater toxicity. This is the first study of the biological effects of LCs on pulmonary epithelia and our observations strongly suggest that LCs pose a more severe danger to human health than cigarettes.

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“…CSE was prepared using a smoke machine as described by previous methods [15,16,17] with some modifications. The direct and side-stream smoke from a cigarette (Fu Rong brand, China) was directed via a tube through 5 ml of DMEM.…”

Section: Methodsmentioning

confidence: 99%

Resveratrol reduces the apoptosis induced by cigarette smoke extract by upregulating MFN2

2017

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PurposeThe aim of this study was to investigate the effect of resveratrol (RSV) on cigarette smoke extract (CSE)-induced cell apoptosis and mitochondrial dysfunction in vitro, as well as changes in the MFN2 expression level.MethodsCultured human bronchial epithelial (HBE) cells were initially treated with CSE to induce apoptosis, followed by incubation either with or without RSV. Numerous techniques were used to evaluate the outcomes of the present study, including a cell counting kit-8 assay, real-time quantitative polymerase chain reaction (real-time qPCR), western blotting, JC-1 fluorescence, Hoechst 33342 staining, Annexin V-PI flow cytometry apoptosis analyses, and siRNA technology.ResultsA 24 h incubation in 3.5% CSE induced apoptosis in HBE cells, and pretreatment of HBE cells with RSV (20 μM) significantly suppressed the CSE-induced apoptosis, prevented the CSE-induced decrease in MFN2 levels, suppressed BAX translocation to the mitochondria, and prevented mitochondrial membrane potential loss and cytochrome C release. However, following the transfection of MFN2 siRNA, the anti-apoptotic effects of RSV were significantly attenuated.ConclusionThe results of the present study demonstrated that RSV may protect bronchial epithelial cells from CS-induced apoptosis in vitro by preventing mitochondrial dysfunction, and MFN2 may be associated with the anti-apoptotic functions of RSV in HBE cells.

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Short- and Long- Term Effects of Cigarette Smoke Exposure on Glutathione Homeostasis in Human Bronchial Epithelial Cells

Cited by 44 publications

References 62 publications

14,15-Epoxyeicosatrienoic Acid Suppresses Cigarette Smoke Extract-Induced Apoptosis in Lung Epithelial Cells by Inhibiting Endoplasmic Reticulum Stress

14,15-Epoxyeicosatrienoic Acid Suppresses Cigarette Smoke Extract-Induced Apoptosis in Lung Epithelial Cells by Inhibiting Endoplasmic Reticulum Stress

Little Cigars are More Toxic than Cigarettes and Uniquely Change the Airway Gene and Protein Expression

Resveratrol reduces the apoptosis induced by cigarette smoke extract by upregulating MFN2

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