Long‐term exposure of human gingival fibroblasts to cigarette smoke condensate reduces cell growth by modulating <scp>B</scp>ax, <scp>c</scp>aspase‐3 and <scp>p</scp>53 expression

Amri, Abdullah Al; Semlali, Abdelhabib; Jacques, Éric; Alanazi, Mohammed M.; Zakrzewski, Andrew; Chmielewski, Witold; Rouabhia, Mahmoud

doi:10.1111/jre.12223

Cited by 25 publications

(22 citation statements)

References 46 publications

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“…Exposure of human cells, such as monocytes and macrophages, to cigarette smoke has been shown to disrupt redox homeostasis (Tanni et al, ), downregulate antioxidant gene expression (Goven et al, ), and enhance pro‐inflammatory responses (Lerner et al, ). Furthermore, the deleterious effect of cigarette smoke on gingival cells has been reported in deregulating gingival fibroblast cell cycle progression by increasing the G 0 /G 1 phase and decreasing the S and G 2 /M phases (Alamri et al, ). Indeed, gene expression analyses showed the activation of several apoptotic genes following exposure to cigarette smoke (Alamri et al, ).…”

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confidence: 99%

E‐Cigarette Vapor Induces an Apoptotic Response in Human Gingival Epithelial Cells Through the Caspase‐3 Pathway

Rouabhia

Park

Semlali

et al. 2016

Journal Cellular Physiology

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Electronic cigarettes represent an increasingly significant proportion of today's consumable tobacco products. E-cigarettes contain several chemicals which may promote oral diseases. The aim of this study was to investigate the effect of e-cigarette vapor on human gingival epithelial cells. Results show that e-cigarette vapor altered the morphology of cells from small cuboidal form to large undefined shapes. Both single and multiple exposures to e-cigarette vapor led to a bulky morphology with large faint nuclei and an enlarged cytoplasm. E-cigarette vapor also increased L-lactate dehydrogenase (LDH) activity in the targeted cells. This activity was greater with repeated exposures. Furthermore, e-cigarette vapor increased apoptotic/necrotic epithelial cell percentages compared to that observed in the control. Epithelial cell apoptosis was confirmed by TUNEL assay showing that exposure to e-cigarette vapor increased apoptotic cell numbers, particularly after two and three exposures. This negative effect involved the caspase-3 pathway, the activity of which was greater with repeated exposure and which decreased following the use of caspase-3 inhibitor. The adverse effects of e-cigarette vapor on gingival epithelial cells may lead to dysregulated gingival cell function and result in oral disease. J. Cell. Physiol. 232: 1539-1547, 2017. © 2016 Wiley Periodicals, Inc.

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confidence: 99%

E‐Cigarette Vapor Induces an Apoptotic Response in Human Gingival Epithelial Cells Through the Caspase‐3 Pathway

Rouabhia

Park

Semlali

et al. 2016

Journal Cellular Physiology

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“…The results were analyzed with a web‐based software (SABiosciences) using the ΔΔ C t method, and the fold changes between the non‐stimulated and CSC‐stimulated samples were calculated. Genes were selected if a fold change above 1.3 was observed and if baseline cycle thresholds for this gene were below 30 to eliminate feebly expressed genes.…”

Section: Methodsmentioning

confidence: 99%

Role of mitogen‐activated protein kinase pathways in migration of gingival epithelial cells in response to stimulation by cigarette smoke condensate and infection by Porphyromonas gingivalis

Imamura

Kokubu

Kita

et al. 2015

J of Periodontal Research

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“…27 Levels of the pro-apoptotic protein Bax, which is involved in triggering ROS production, is up-regulated by CSE. 30 Bax expression was also elevated after exposure to nicotine-containing and nicotine-free E-liquids and vapours for 24 hours, followed by cell apoptosis after 48 hours. 27 The epithelium forms the first line of defence against toxic substances and periodontal pathogens.…”

Section: F I G U R E 2 Effects Of Electronic Cigarettes In Humansmentioning

confidence: 96%

“…Similarly, ROS production was increased significantly after 24‐hour exposure of gingival fibroblasts to either nicotine‐containing or nicotine‐free fluids and vapours, indicating that nicotine was not the only inducer of ROS production . Levels of the pro‐apoptotic protein Bax, which is involved in triggering ROS production, is up‐regulated by CSE . Bax expression was also elevated after exposure to nicotine‐containing and nicotine‐free E‐liquids and vapours for 24 hours, followed by cell apoptosis after 48 hours …”

Section: Effects Of E‐cigarettes In Humansmentioning

confidence: 98%

Immunological and pathological effects of electronic cigarettes

Chen

Todd

Fairclough

2019

Basic Clin Pharma Tox

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Electronic cigarettes (E‐cigarettes) are considered a preferable alternative to conventional cigarettes due to the lack of combustion and the absence of tobacco‐specific toxicants. E‐cigarettes have rapidly gained in popularity in recent years amongst both existing smokers and previous non‐smokers. However, a growing literature demonstrates that E‐cigarettes are not as safe as generally believed. Here, we discuss the immunological, and other, deleterious effects of E‐cigarettes on a variety of cell types and host defence mechanisms in humans and in murine models. We review not only the effects of complete E‐cigarette liquids, but also each of the main components—nicotine, humectants and flavourings. This MiniReview thus highlights the possible role of E‐cigarettes in the pathogenesis of disease and raises awareness of the potential harm that E‐cigarettes may cause.

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Long‐term exposure of human gingival fibroblasts to cigarette smoke condensate reduces cell growth by modulating Bax, caspase‐3 and p53 expression

Abstract: These results suggest that CSC may contribute to deregulating fibroblast functions. This can compromise fibroblast-epithelial cell interactions, which ultimately increases the risk of gingival tissue damage and the onset of periodontitis.

Cited by 25 publications

References 46 publications

E‐Cigarette Vapor Induces an Apoptotic Response in Human Gingival Epithelial Cells Through the Caspase‐3 Pathway

E‐Cigarette Vapor Induces an Apoptotic Response in Human Gingival Epithelial Cells Through the Caspase‐3 Pathway

Role of mitogen‐activated protein kinase pathways in migration of gingival epithelial cells in response to stimulation by cigarette smoke condensate and infection by Porphyromonas gingivalis

Immunological and pathological effects of electronic cigarettes

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