scholarly journals Calcium-dependent and independent mechanisms of capsaicin receptor (TRPV1)-mediated cytokine production and cell death in human bronchial epithelial cells

2005 ◽  
Vol 19 (4) ◽  
pp. 266-275 ◽  
Author(s):  
Christopher A. Reilly ◽  
Mark E. Johansen ◽  
Diane L. Lanza ◽  
Jeewoo Lee ◽  
Ju-Ok Lim ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Cytokine Production ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Capsaicin Receptor ◽  
Calcium Dependent

scholarly journals Additive effects of simulated microgravity and ionizing radiation in cell death, induction of ROS and expression of RAC2 in human bronchial epithelial cells

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Shaobo Tan ◽  
Weiwei Pei ◽  
Hao Huang ◽  
Guangming Zhou ◽  
Wentao Hu
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Ionizing Radiation ◽  
Simulated Microgravity ◽  
Biological Effects ◽  
Bronchial Epithelial Cells ◽  
Space Environment ◽  
Mechanistic Study ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

Abstract Radiation and microgravity are undoubtedly two major factors in space environment that pose a health threat to astronauts. However, the mechanistic study of their interactive biological effects is lacking. In this study, human lung bronchial epithelial Beas-2B cells were used to study the regulation of radiobiological effects by simulated microgravity (using a three-dimensional clinostat). It was found that simulated microgravity together with radiation induced drop of survival fraction, proliferation inhibition, apoptosis, and DNA double-strand break formation of Beas-2B cells additively. They also additively induced Ras-related C3 botulinum toxin substrate 2 (RAC2) upregulation, leading to increased NADPH oxidase activity and increased intracellular reactive oxygen species (ROS) yield. The findings indicated that simulated microgravity and ionizing radiation presented an additive effect on cell death of human bronchial epithelial cells, which was mediated by RAC2 to some extent. The study provides a new perspective for the better understanding of the compound biological effects of the space environmental factors.

scholarly journals Tiotropium/Olodaterol Reduce Cigarette Smoking 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 Smoking ◽  
Cell Injury ◽  
Lung Parenchyma ◽  
Underlying Mechanism ◽  
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.

SWCNTs induced autophagic cell death in human bronchial epithelial cells

2014 ◽  
Vol 28 (3) ◽  
pp. 442-450 ◽  
Author(s):  
Eun-Jung Park ◽  
Nur Elida M. Zahari ◽  
Eun-Woo Lee ◽  
Jaewhan Song ◽  
Jae-Hyeok Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Autophagic Cell Death ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

Uptake of 12-HETE by human bronchial epithelial cells (HBEC): Effects on HBEC cytokine production

1996 ◽  
Vol 51 (4) ◽  
pp. 263-273 ◽  
Author(s):  
Frederic Gormand ◽  
Bernard Chabannes ◽  
Patrick Moliere ◽  
Max Perrin-Fayolle ◽  
Michel Lagarde ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cytokine Production ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial
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