Actin re-distribution in response to hydrogen peroxide in airway epithelial cells

2004 ◽  
Vol 199 (1) ◽  
pp. 57-66 ◽  
Author(s):  
Kendrick C. Boardman ◽  
Ashish M. Aryal ◽  
William M. Miller ◽  
Christopher M. Waters
Keyword(s):  
Hydrogen Peroxide ◽  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial

scholarly journals Effects of hydrogen peroxide on mucociliary transport in human airway epithelial cells

2014 ◽  
Vol 24 (3) ◽  
pp. 191-195 ◽  
Author(s):  
Akiko Honda ◽  
Rumiko Murayama ◽  
Yugo Matsuda ◽  
Kenshi Tsuji ◽  
Takahiro Sawahara ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Mucociliary Transport ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cells

Argon Preconditioning Protects Airway Epithelial Cells against Hydrogen Peroxide-Induced Oxidative Stress

2016 ◽  
Vol 57 (3-4) ◽  
pp. 252-262 ◽  
Author(s):  
Christina Hafner ◽  
Hong Qi ◽  
Lourdes Soto-Gonzalez ◽  
Katharina Doerr ◽  
Roman Ullrich ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Apoptotic Cell ◽  
A549 Cells ◽  
Airway Epithelial Cells ◽  
Cerebral Injury ◽  
Mitogen Activated Protein Kinase ◽  
Airway Epithelial

Background: Oxidative stress is the predominant pathogenic mechanism of ischaemia-reperfusion (IR) injury. The noble gas argon has been shown to alleviate oxidative stress-related myocardial and cerebral injury. The risk of lung IR injury is increased in some major surgeries, reducing clinical outcome. However, no study has examined the lung-protective efficacy of argon preconditioning. The present study investigated the protective effects of argon preconditioning on airway epithelial cells exposed to hydrogen peroxide (H2O2) to induce oxidative stress. Methods: A549 airway epithelial cells were treated with a cytotoxic concentration of H2O2 after exposure to standard air or 30 or 50% argon/21% oxygen/5% carbon dioxide/rest nitrogen for 30, 45 or 180 min. Cells were stained with annexin V/propidium iodide, and apoptosis was evaluated by fluorescence-activated cell sorting. Protective signalling pathways activated by argon exposure were identified by Western blot analysis for phosphorylated candidate molecules of the mitogen-activated protein kinase and protein kinase B (Akt) pathways. Results: Preconditioning with 50% argon for 30, 45 and 180 min and 30% argon for 180 min caused significant protection of A549 cells against H2O2-induced apoptosis, with increases in cellular viability of 5-47% (p < 0.0001). A small adverse effect was also observed, which presented as a 12-15% increase in cellular necrosis in argon-treated groups. Argon exposure resulted in early activation of c-Jun N-terminal kinase (JNK) and p38, peaking 10- 30 min after the start of preconditioning, and delayed activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, peaking after 60-90 min. Conclusions: Argon preconditioning protects airway epithelial cells from H2O2-induced apoptotic cell death. Argon activates the JNK, p38, and ERK1/2 pathways, but not the Akt pathway. The cytoprotective properties of argon suggest possible prophylactic applications in surgery-related IR injury of the lungs.

Visualization of labile zinc and its role in apoptosis of primary airway epithelial cells and cell lines

2000 ◽  
Vol 279 (6) ◽  
pp. L1172-L1183 ◽  
Author(s):  
Ai Q. Truong-Tran ◽  
Richard E. Ruffin ◽  
Peter D. Zalewski
Keyword(s):  
Hydrogen Peroxide ◽  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Zn Deficiency ◽  
The Novel ◽  
Airway Epithelial ◽  
Caspase Activation ◽  
Respiratory Epithelial Cells ◽  
Upper Respiratory ◽  
Respiratory Epithelial

The respiratory epithelium is vulnerable to noxious substances, resulting in the shedding of cells and decreased protection. Zinc (Zn), an antioxidant and cytoprotectant, can suppress apoptosis in a variety of cells. Here we used the novel Zn-specific fluorophore Zinquin to visualize and quantify labile intracellular Zn in respiratory epithelial cells. Zinquin fluorescence in isolated ciliated tracheobronchial epithelial cells and intact epithelium from sheep and pigs revealed an intense fluorescence in the apical and mitochondria-rich cytoplasm below the cilia. Zinquin fluorescence was quenched by the Zn chelator N, N, N′, N′-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) and increased by the Zn ionophore pyrithione. We also assessed whether changes in intracellular labile Zn would influence susceptibility of these cells to apoptosis by hydrogen peroxide. Our results confirm that Zn deficiency enhanced hydrogen peroxide-induced caspase activation from 1.24 ± 0.12 to 2.58 ± 0.53 units · μg protein−1· h−1( P ≤ 0.05); Zn supplementation suppressed these effects. These findings are consistent with the hypothesis that Zn protects upper respiratory epithelial cells and may have implications for human asthma where there is hypozincemia and epithelial damage.

Continuous exposure of airway epithelial cells to hydrogen peroxide: Protection by KGF

2002 ◽  
Vol 192 (1) ◽  
pp. 71-80 ◽  
Author(s):  
Kenneth E. Chapman ◽  
Christopher M. Waters ◽  
William M. Miller
Keyword(s):  
Hydrogen Peroxide ◽  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Continuous Exposure ◽  
Airway Epithelial
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