Modifications in Human Oral Fibroblast Ultrastructure, Collagen Production, and Lysosomal Compartment in Response to Electronic Cigarette Fluids

Sancilio, Silvia; Gallorini, M.; Cataldi, Amelia; Sancillo, Laura; Rana, Rosa Alba; Giacomo, Viviana di

doi:10.1902/jop.2017.160629

Cited by 21 publications

(23 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the present study, we observed that chronic nicotine exposure enhanced autophagy biomarkers (such as LC3II, p62, Beclin 1, and Atg 5) protein abundance in cardiac tissues. Consistent with our observation, other studies have shown that nicotine exposure increases autophagy activation in human fibroblast cells [31], human cancer colon cells [32], and bronchial epithelial cells [13]. These findings suggest that nicotine is one of the key activators of autophagy.…”

Section: Discussionsupporting

confidence: 93%

Inhibition of Autophagy Signaling via 3-methyladenine Rescued Nicotine-Mediated Cardiac Pathological Effects and Heart Dysfunctions

Zhang¹,

Li²,

Fu³

et al. 2020

Int. J. Biol. Sci.

View full text Add to dashboard Cite

Rationale: Cigarette smoking is a well-established risk factor for myocardial infarction and sudden cardiac death. The deleterious effects are mainly due to nicotine, but the mechanisms involved and theranostics remain unclear. Thus, we tested the hypothesis that nicotine exposure increases the heart sensitivity to ischemia/reperfusion injury and dysfunction, which can be rescued by autophagy inhibitor. Methods: Nicotine or saline was administered to adult rats via subcutaneous osmotic minipumps in the absence or presence of an autophagy inhibitor, 3-methyladenine (3-MA). After 30 days of nicotine treatment, the rats underwent the cardiac ischemia/reperfusion (I/R) procedure and echocardiography analysis, and the heart tissues were isolated for molecular biological studies. Results: Nicotine exposure increased I/R-induced cardiac injury and cardiac dysfunction as compared to the control. The levels of autophagy-related proteins including LC3 II, P62, Beclin1, and Atg5 were upregulated in the reperfused hearts isolated from nicotine-treated group. In addition, nicotine enhanced cardiac and plasma ROS production, and increased the phosphorylation of GSK3β (ser9) in the left ventricle tissues. Treatment with 3-MA abolished nicotine-mediated increase in the levels of autophagy-related proteins and phosphorylation of GSK3β, but had no effect on ROS production. Of importance, 3-MA ameliorated the augmented I/R-induced cardiac injury and dysfunction in the nicotine-treated group as compared to the control. Conclusion: Our results demonstrate that nicotine exposure enhances autophagy signaling pathway, resulting in development of ischemic-sensitive phenotype of heart. It suggests a potentially novel therapeutic strategy of autophagy inhibition for the treatment of ischemic heart disease.

show abstract

Section: Discussionsupporting

confidence: 93%

Inhibition of Autophagy Signaling via 3-methyladenine Rescued Nicotine-Mediated Cardiac Pathological Effects and Heart Dysfunctions

Zhang¹,

Li²,

Fu³

et al. 2020

Int. J. Biol. Sci.

View full text Add to dashboard Cite

show abstract

“…The nicotine‐containing treatment in our collagen type I RNA and protein experiments had a concentration of 620 μ m (0.1 mg/mL), which falls in between these previous reports, although it is below the 1 m m concentration reported to result in downregulation. Consistent with the biphasic nature of nicotine, when human oral fibroblasts are exposed to unvaped e‐liquid containing 6.2 m m nicotine for 24 hours there is a decrease in collagen type I protein (Sancilio et al, ). In addition to nicotine, the flavorings alone may alter osteoblast gene expression.…”

Section: Discussionmentioning

confidence: 85%

Electronic cigarette liquid exposure induces flavor‐dependent osteotoxicity and increases expression of a key bone marker, collagen type I

Otero

Noeker

Brown

et al. 2019

J of Applied Toxicology

View full text Add to dashboard Cite

Electronic cigarettes (e‐cigarettes) are nicotine delivery devices advertised as a healthier alternative to conventional tobacco products, but their rapid rise in popularity outpaces research on potential health consequences. As conventional tobacco use is a risk factor for osteoporosis, this study examines whether exposure to electronic liquid (e‐liquid) used in e‐cigarettes affects bone‐forming osteoblasts. Human MG‐63 and Saos‐2 osteoblast‐like cells were treated for 48 hours with 0.004%‐4.0% dilutions of commercially available e‐liquids of various flavors with or without nicotine. Changes in cell viability and key osteoblast markers, runt‐related transcription factor 2 and Col1a1, were assessed. With all e‐liquids tested, cell viability decreased in a dose‐dependent manner, which was least pronounced in flavorless e‐liquids, most pronounced in cinnamon‐flavored e‐liquids and occurred independently of nicotine. Col1a1, but not runt‐related transcription factor 2, mRNA expression was upregulated in response to coffee‐flavored and fruit‐flavored e‐liquids. Cells treated with a non‐cytotoxic concentration of fruit‐flavored Mango Blast e‐liquid with or without nicotine showed significantly increased collagen type I protein expression compared to culture medium only. We conclude that the degree of osteotoxicity is flavor‐dependent and occurs independently of nicotine and that flavored e‐liquids reveal collagen type I as a potential target in osteoblasts. This study elucidates potential consequences of e‐cigarette use in bone.

show abstract

“…Results from recent studies showed that cigarette smoke could induce the autophagy in cells from periodontal tissues (Du et al, ; Kim et al, ; Moga et al, ; Sancilio et al, ; Table ). Moga et al reported that nicotine could induce the presence of autophagosomes in mesenchymal stem cells from human periodontium (including gingival ligament stem cells, periodontal ligament stem cells, gingival tissue stem cells, and alveolar bone stem cells) at intermediate doses (0.622–3.112 μM; Moga et al, ).…”

Section: Autophagy and Cigarette Smokementioning

confidence: 99%

“…Sancilio et al found that cigarette fluids, no matter with or without nicotine, could induce the presence of autophagic vesicles, but the expression of LC3 and the release of collagen could not be regulated by cigarette fluid without nicotine in HGFs. It was suggested that the cigarette without nicotine might regulate autophagy via cellular morphologic response (Sancilio et al, ).…”

Section: Autophagy and Cigarette Smokementioning

confidence: 99%

See 1 more Smart Citation

The role of autophagy in the pathogenesis of periodontal disease

Jiang

Zhu

2019

Oral Diseases

View full text Add to dashboard Cite

Periodontal disease is a chronic inflammatory disease leading to destruction of periodontal tissues. As a local inflammation, periodontopathic bacterium, pro‐inflammatory mediators, and local immune response play pivotal role in the progress of periodontal disease. Besides, cigarette smoke has long been associated with periodontal disease and tooth loss. Autophagy is an intracellular degradation process highly conserved from yeast to humans. As a lysosomal degradation pathway of self‐digestion, it is critical for maintaining cells homeostasis and development. The role of autophagy has been investigated in oral diseases, such as oral cancer, periapical lesions, and oral candidiasis. Recently, increasing studies investigated the role of autophagy in periodontal disease. In this review, we try to illustrate the effect of autophagy on periodontal disease pathogenesis from 5 aspects: autophagy affects the intracellular infection and survival of bacteria; autophagy has an interaction with periodontal inflammation; autophagy is pivotal in periodontal cells biology and periodontal tissues destruction and reconstruction; autophagy can be induced by cigarette smoke; last but not least, autophagy may affect periodontal disease via endoplasmic reticulum stress.

show abstract

Modifications in Human Oral Fibroblast Ultrastructure, Collagen Production, and Lysosomal Compartment in Response to Electronic Cigarette Fluids

Abstract: E-cigarette fluids (with and without nicotine) trigger molecular and morphologic responses in oral fibroblasts, raising concerns about their role in the pathogenesis of oral diseases.

Cited by 21 publications

References 34 publications

Inhibition of Autophagy Signaling via 3-methyladenine Rescued Nicotine-Mediated Cardiac Pathological Effects and Heart Dysfunctions

Inhibition of Autophagy Signaling via 3-methyladenine Rescued Nicotine-Mediated Cardiac Pathological Effects and Heart Dysfunctions

Electronic cigarette liquid exposure induces flavor‐dependent osteotoxicity and increases expression of a key bone marker, collagen type I

The role of autophagy in the pathogenesis of periodontal disease

Contact Info

Product

Resources

About