scholarly journals Cigarette smoke extract and heated tobacco products promote ferritin cleavage and iron accumulation in human corneal epithelial cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Wataru Otsu ◽  
Kodai Ishida ◽  
Naoki Chinen ◽  
Shinsuke Nakamura ◽  
Masamitsu Shimazawa ◽  
...  
Keyword(s):  
Cell Death ◽  
T Cell ◽  
Epithelial Cell ◽  
Cigarette Smoke ◽  
Cell Injury ◽  
Cigarette Smoke Extract ◽  
Corneal Epithelial Cell ◽  
Dependent Manner ◽  
Tobacco Products ◽  
Corneal Epithelial

AbstractThe cornea is directly exposed to cigarette smoke, and smoking is a risk factor for several corneal diseases including dry eye syndrome. Currently, heated tobacco products (HTPs) are widely used as substitutes for cigarette smoking around the world. In the present study, we investigated the molecular mechanism(s) leading to cellular injury induced by cigarette smoke extract (CSE) or HTPs. Exposure to CSE perturbed the formation of tight junctions, leading to an increase in cell volume, a decrease in transepithelial electrical resistance (TER) in the human corneal epithelial cell-transformed (HCE-T) cell line. Moreover, CSE exposure induced both lipid peroxidation and ferrous [Fe(II)] ion accumulation in autolysosomal compartments. Interestingly, a cleaved form of ferritin appeared when HCE-T cells were incubated with CSE. This aberrant ferritin processing was suppressed by treatment with autophagy inhibitors. Furthermore, the CSE-induced cell death was suppressed by either ferrostatin-1 or deferoxamine (DFO). CSE exposure also promoted the expression of cytokines whereas DFO treatment inhibited the CSE-induced expression of these cytokines. Exposure to HTPs also induced both HCE-T cell death and cleaved ferritin accumulation in a concentration- and time-dependent manner. These results indicated that CSE or HTPs activated the ferroptosis signaling pathway, which contributed to corneal epithelial cell injury.

Inhibition of microRNA‐129‐5p expression ameliorates ultraviolet ray‐induced corneal epithelial cell injury via upregulation of EGFR

2018 ◽  
Vol 234 (7) ◽  
pp. 11692-11707 ◽  
Author(s):  
Ying Yang ◽  
Bo Gong ◽  
Zheng‐Zheng Wu ◽  
Ping Shuai ◽  
Dong‐Feng Li ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Injury ◽  
Corneal Epithelial Cell ◽  
Corneal Epithelial ◽  
Ultraviolet Ray ◽  
Epithelial Cell Injury

scholarly journals Tiotropium/Olodaterol Treatment Reduces Cigarette Smoke Extract-induced Cell Death in BEAS-2B Bronchial Epithelial Cells

2020 ◽  
Author(s):  
Cheng-Hsiung Chen ◽  
Yi-Rong Li ◽  
Sheng-Hao Lin ◽  
Hsiu-Hui Chang ◽  
Woei-Horng Chai ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Cell Injury ◽  
Underlying Mechanism ◽  
Cigarette Smoke Extract ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Jnk Activation

Abstract Background: Cigarette smoking is a critical risk factor for the destruction of lung parenchyma or the development of emphysema, which is characteristic of COPD. Disruption of epithelial layer integrity may contribute to lung injury following cigarette smoke extract (CSE) exposure. Tiotropium/olodaterol acts as a bronchodilator for COPD treatment; however, the effect of dual bronchodilators on epithelial cell injury and its underlying mechanism remain unclear. In this study, we evaluated the effect of tiotropium/olodaterol on CSE-mediated cell death and the underlying mechanisms.Methods: Cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis, necrosis, and autophagy were evaluated using flow cytometry. Autophagy-related protein, phosphorylated ERK, expression was determined using Western blotting.Results: Tiotropium/olodaterol significantly inhibited CSE-induced cell death, mitochondria dysfunction, and autophagy, which had no significant effect on apoptosis or necrosis in BEAS-2B human bronchial epithelial cells. Moreover, tiotropium/olodaterol attenuated CSE-induced upregulation of JNK.Conclusions: CSE induced cell death and caused consistent patterns of autophagy and JNK activation in BEAS-2B human bronchial epithelial cells. Tiotropium/olodaterol treatment protected bronchial epithelial cells from CSE-induced injury and inhibited activation of autophagy and upregulation of JNK phosphorylation. These results indicate that tiotropium/olodaterol may protect epithelial cells from the deleterious effects of CSE exposure, which is associated with the regulation of autophagy and JNK activation.

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