Mitochondrial dysfunction is associated with Miro1 reduction in lung epithelial cells by cigarette smoke

Sundar, Isaac K.; Maremanda, Krishna Prahlad; Rahman, Irfan

doi:10.1016/j.toxlet.2019.09.022

Cited by 49 publications

(62 citation statements)

References 38 publications

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“…Therefore, cigarette smoking extract is logical choice to experimentally explore the mechanism and pathogenesis of COPD in vitro. Moreover, there are accumulative evidence indicated that cigarette smoking-induce lung injury is related to epithelial cell disruption [6,8,9,12]. In present study, we also demonstrate CSE treatment cause cell death in lung epithelial cell.…”

Section: Discussionsupporting

confidence: 73%

“…Recently, several evidences suggest that increased autophagy contributes to COPD pathogenesis. In vitro studies demonstrated that autophagy activation contribute to CS-induced cilia shortening and mitochondrial dysfunction in airway epithelium as well [11,12]. Moreover, cigarette smoke induced epithelial cell through activating autophagy via modulating various signaling pathway were identified [9,10,13,14].…”

Section: Introductionmentioning

confidence: 99%

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Tiotropium/Olodaterol Reduce Cigarette Smoking Extract-induced Cell Death in BEAS-2B Bronchial Epithelial Cells

Chen

Lin

et al. 2020

Preprint

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Background COPD is characterized by progressive irreversible airflow limitation. Cigarette smoking is an important risk factor for destruction of lung parenchyma or emphysema. Disruption of epithelial layer integrity may contribute to lung injury in response to CS exposure. Tiotropium/Olodaterol act as bronchodilator to treatment COPD by preventing ASM contraction and muscle relaxation; however, the effect of dual bronchodilator on epithelial cell injury and its underlying mechanism is still unclear. In this study, we aim to evaluate the effect of Tiotropium/Olodaterol on CSE-mediate cell death, with a special focus on autophagy.Methods In this study, we investigated the effects of Tiotropium/Olodaterol on cell viability, the mitochondrial membrane potential (MMP; Δφm), and autophagy in BEAS-2B bronchial epithelial cells. Result: Tiotropium/olodaterol significantly inhibit CSE-induce cell death, mitochondria dysfunction and autophagy in response to short-term treatment with CSE. Moreover, decrease in ERK and JNK activation after CSE treatment were reversed by Tiotropium/olodaterol treatment. Conclusion: Tiotropium/olodaterol have protective effect against CSE-induced cell death which may related to induction of autophagy via activating ERK and JNK. In this study, we provide a possible novel mechanism for dual bronchodilator in COPD treatment.

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Section: Discussionsupporting

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Tiotropium/Olodaterol Reduce Cigarette Smoking Extract-induced Cell Death in BEAS-2B Bronchial Epithelial Cells

Chen

Lin

et al. 2020

Preprint

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“…Pod-based e-juices and flavors also induce cellular toxicity with identification of several toxic chemicals , hence this will render users susceptible to further damage as seen in EVALI cases. Similarly, Wang et al reported dysregulated lung repair following E-cig exposure (Sundar et al, 2019). Whereas in a long-term exposure (3-6 mo) study using the two strains of mice, higher levels of Angiopoietin-1 and CXCL5 were observed along with lower MMP3 levels, indicating the involvement of the tissue-remodeling pathways (Crotty Alexander et al, 2018).…”

Section: Disussion On Cellular and Molecular Mechanisms Of Evalimentioning

confidence: 93%

Pulmonary Toxicity and the Pathophysiology of Electronic Cigarette, or Vaping Product, Use Associated Lung Injury

et al. 2020

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New emerging tobacco products, especially electronic cigarettes (E-Cig) or electronic nicotine delivery systems (ENDS), have gained a huge popularity, particularly in younger populations. The lack of sufficient evidence-based health effect studies has promoted widespread use/abuse with the assumption that E-Cig or ENDS and/or vaping products are safer and less toxic than conventional tobacco smoking. However, the recent escalation in acute lung injuries and their associated fatalities among ENDS or vaping product users has now brought attention to this silent epidemic via investigation into the constituents of ENDS/vaping products and their toxic effects on pulmonary health. Accordingly, CDC has declared an "outbreak" of the e-cigarette or vaping product use associated lung injury (EVALI). EVALI is characterized by sterile exogenous pneumonitis like reaction with substantial involvement of innate immune mechanisms. Vitamin-E acetate (VEA) is found in counterfeit cartridges and bronchoalveolar lavage fluid of EVALI patients. Other reports implicated the presence of aromatic/volatile hydrocarbons and oils consisting of medium-chain triglycerides (MCT oil), including terpenes and mineral oil in tetrahydrocannabinol (THC) containing counterfeit vaping products. These compounds are involved in oxidative stress and inflammatory responses in the lung. Here, we provide the perspectives on the recent case reports on EVALI, etiology, and discuss pulmonary toxicity as well as the mechanisms underlying EVALI susceptibility and lung pathophysiology.

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“…Cigarette smoking is the major cause of irreversible lung diseases, including COPD and emphysema. Increasing evidence has indicated that cigarette smoking–induced lung injury is related to epithelial cell disruption [ 6 , 8 , 9 , 17 ]. A combination of tiotropium and olodaterol is used as long-term maintenance treatment for COPD, including chronic bronchitis or emphysema [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Tiotropium/Olodaterol treatment reduces cigarette smoke extract-induced cell death in BEAS-2B bronchial epithelial cells

Chen

Lin

et al. 2020

BMC Pharmacol Toxicol

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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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Mitochondrial dysfunction is associated with Miro1 reduction in lung epithelial cells by cigarette smoke

Cited by 49 publications

References 38 publications

Tiotropium/Olodaterol Reduce Cigarette Smoking Extract-induced Cell Death in BEAS-2B Bronchial Epithelial Cells

Tiotropium/Olodaterol Reduce Cigarette Smoking Extract-induced Cell Death in BEAS-2B Bronchial Epithelial Cells

Pulmonary Toxicity and the Pathophysiology of Electronic Cigarette, or Vaping Product, Use Associated Lung Injury

Tiotropium/Olodaterol treatment reduces cigarette smoke extract-induced cell death in BEAS-2B bronchial epithelial cells

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