scholarly journals Zinc oxide nanoparticles harness autophagy to induce cell death in lung epithelial cells

2017 ◽  
Vol 8 (7) ◽  
pp. e2954-e2954 ◽  
Author(s):  
Jun Zhang ◽  
Xia Qin ◽  
Bin Wang ◽  
Ge Xu ◽  
Zhexue Qin ◽  
...  
Keyword(s):  
Cell Death ◽  
Zinc Oxide ◽  
Epithelial Cells ◽  
Zinc Oxide Nanoparticles ◽  
Lung Epithelial Cells ◽  
Oxide Nanoparticles ◽  
Induce Cell Death ◽  
Lung Epithelial

Characterization of Nitric Oxide (NO)-Induced Cell Death in Lung Epithelial Cells

2004 ◽  
Vol 56 (2) ◽  
pp. 187
Author(s):  
Wha Shim Yong ◽  
Youn Seup Kim ◽  
Jae Seuk Park ◽  
Young Koo Jee ◽  
Kye Young Lee
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

scholarly journals Size-dependent cytotoxicity of copper oxide nanoparticles in lung epithelial cells

2016 ◽  
Vol 3 (2) ◽  
pp. 365-374 ◽  
Author(s):  
Amaraporn Wongrakpanich ◽  
Imali A. Mudunkotuwa ◽  
Sean M. Geary ◽  
Angie S. Morris ◽  
Kranti A. Mapuskar ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Copper Oxide ◽  
Copper Oxide Nanoparticles ◽  
Cuo Nanoparticles ◽  
Lung Epithelial Cells ◽  
Oxide Nanoparticles ◽  
Size Dependent ◽  
Lung Epithelial

The increasing use of copper oxide (CuO) nanoparticles (NPs) in medicine and industry demands an understanding of their potential toxicities.

scholarly journals Induction of Cell Death through Alteration of Oxidants and Antioxidants in Lung Epithelial Cells Exposed to High Energy Protons

2010 ◽  
Vol 285 (32) ◽  
pp. 24769-24774 ◽  
Author(s):  
Sudhakar Baluchamy ◽  
Prabakaran Ravichandran ◽  
Adaikkappan Periyakaruppan ◽  
Vani Ramesh ◽  
Joseph C. Hall ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
High Energy ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

scholarly journals F-Box Protein FBXW17-Mediated Proteasomal Degradation of Protein Methyltransferase PRMT6 Exaggerates CSE-Induced Lung Epithelial Inflammation and Apoptosis

2021 ◽  
Vol 9 ◽  
Author(s):  
Tiao Li ◽  
Xue He ◽  
Lijuan Luo ◽  
Huihui Zeng ◽  
Siying Ren ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Cigarette Smoke ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Lung Epithelial Cells ◽  
Chronic Obstructive ◽  
Structural Cell ◽  
Lung Epithelial

Chronic obstructive pulmonary disease (COPD) is a chronic debilitating lung disease, characterized by progressive airway inflammation and lung structural cell death. Cigarette smoke is considered the most common risk factor of COPD pathogenesis. Understanding the molecular mechanisms of persistent inflammation and epithelial apoptosis induced by cigarette smoke would be extremely beneficial for improving the treatment and prevention of COPD. A histone methyl modifier, protein arginine N-methyltransferase 6 (PRMT6), is reported to alleviate cigarette smoke extract (CSE)-induced emphysema through inhibiting inflammation and cell apoptosis. However, few studies have focused on the modulation of PRMT6 in regulating inflammation and cell apoptosis. In this study, we showed that protein expression of PRMT6 was aberrantly decreased in the lung tissue of COPD patients and CSE-treated epithelial cells. FBXW17, a member of the Skp1-Cullin-F-box (SCF) family of E3 ubiquitin ligases, selectively bound to PRMT6 in nuclei to modulate its elimination in the proteasome system. Proteasome inhibitor or silencing of FBXW17 abrogated CSE-induced PRMT6 protein degradation. Furthermore, negative alteration of FBXW17/PRMT6 signaling lessened the proapoptotic and proinflammatory effects of CSE in lung epithelial cells. Our study, therefore, provides a potential therapeutic target against the airway inflammation and cell death in CS-induced COPD.

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