scholarly journals Dexmedetomidine Attenuates Oxidative Stress Induced Lung Alveolar Epithelial Cell ApoptosisIn Vitro

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Jian Cui ◽  
Hailin Zhao ◽  
Chunyan Wang ◽  
James J. Sun ◽  
Kaizhi Lu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Epithelial Cell ◽  
Cell Cycle Arrest ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial Cells ◽  
Epithelial Cell Line ◽  
Alveolar Epithelial ◽  
Cycle Arrest ◽  
E Cadherin

Background. Oxidative stress plays a pivotal role in the lung injuries of critical ill patients. This study investigates the protection conferred byα2adrenoceptor agonist dexmedetomidine (Dex) from lung alveolar epithelial cell injury induced by hydrogen peroxide (H2O2) and the underlying mechanisms.Methods. The lung alveolar epithelial cell line, A549, was cultured and then treated with 500 μM H2O2with or without Dex (1 nM) or Dex in combination with atipamezole (10 nM), an antagonist ofα2receptors. Their effect on mitochondrial membrane potential (Δψm), reactive oxygen species (ROS), and the cell cycle was assessed by flow cytometry. Cleaved-caspases 3 and 9, BAX, Bcl-2, phospho-mTOR (p-mTOR), ERK1/2, and E-cadherin expression were also determined with immunocytochemistry.Results. Upregulation of cleaved-caspases 3 and 9 and BAX and downregulation of Bcl-2, p-mTOR, and E-cadherin were found following H2O2treatment, and all of these were reversed by Dex. Dex also prevented the ROS generation, cytochrome C release, and cell cycle arrest induced by H2O2. The effects of Dex were partially reversed by atipamezole.Conclusion. Our study demonstrated that Dex protected lung alveolar epithelial cells from apoptotic injury, cell cycle arrest, and loss of cell adhesion induced by H2O2through enhancing the cell survival and proliferation.

scholarly journals Ambient particulate matter induces alveolar epithelial cell cycle arrest: Role of G1 cyclins

FEBS Letters ◽  
2007 ◽  
Vol 581 (27) ◽  
pp. 5315-5320 ◽  
Author(s):  
Jingmei Zhang ◽  
Andrew J. Ghio ◽  
Mingxing Gao ◽  
Ke Wei ◽  
Glenn D. Rosen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Particulate Matter ◽  
Epithelial Cell ◽  
Cell Cycle Arrest ◽  
Alveolar Epithelial Cell ◽  
Ambient Particulate Matter ◽  
Alveolar Epithelial ◽  
G1 Cyclins ◽  
Cycle Arrest

scholarly journals Mechanisms of suppression of alveolar epithelial cell GM-CSF expression in the setting of hyperoxic stress

2010 ◽  
Vol 298 (3) ◽  
pp. L446-L453 ◽  
Author(s):  
Anne Sturrock ◽  
Timothy Vollbrecht ◽  
Mustafa Mir-Kasimov ◽  
Michael McManus ◽  
Steven E. Wilcoxen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
Alveolar Epithelial Cell ◽  
Primary Cultures ◽  
Immune Defense ◽  
Serum Deprivation ◽  
Alveolar Epithelial Cells ◽  
Epithelial Cell Line ◽  
Alveolar Epithelial ◽  
Gm Csf

Pulmonary expression of granulocyte/macrophage colony-stimulating factor (GM-CSF) is critically important for normal functional maturation of alveolar macrophages. We found previously that lung GM-CSF is dramatically suppressed in mice exposed to hyperoxia. Alveolar epithelial cells (AEC) are a major source of GM-CSF in the peripheral lung, and in vivo hyperoxia resulted in greatly reduced expression of GM-CSF protein by AEC ex vivo. We now explore the mechanisms responsible for this effect, using primary cultures of murine AEC exposed to hyperoxia in vitro. Exposure of AEC to 80% oxygen/5% CO2 for 48 h did not induce overt toxicity, but resulted in significantly decreased GM-CSF protein and mRNA expression compared with cells in normoxia. Similar effects were seen when AEC were stressed with serum deprivation, an alternative inducer of oxidative stress. The effects in AEC were opposite those in a murine lung epithelial cell line (MLE-12 cells), in which hyperoxia induced GM-CSF expression. Both hyperoxia and serum deprivation resulted in increased intracellular reactive oxygen species (ROS) in AEC. Hyperoxia and serum deprivation induced significantly accelerated turnover of GM-CSF mRNA. Treatment of AEC with catalase during oxidative stress preserved GM-CSF protein and mRNA and was associated with stabilization of GM-CSF mRNA. We conclude that hyperoxia-induced suppression of AEC GM-CSF expression is a function of ROS-induced destabilization of GM-CSF mRNA. We speculate that AEC oxidative stress results in significantly impaired pulmonary innate immune defense due to effects on local GM-CSF expression in the lung.

scholarly journals Bleomycin Inhibits Proliferation via Schlafen-Mediated Cell Cycle Arrest in Mouse Alveolar Epithelial Cells

2019 ◽  
Vol 82 (2) ◽  
pp. 133 ◽  
Author(s):  
Soojin Jang ◽  
Se Min Ryu ◽  
Jooyeon Lee ◽  
Hanbyeol Lee ◽  
Seok-Ho Hong ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Epithelial Cells ◽  
Cell Cycle Arrest ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial ◽  
Cycle Arrest

Cytotoxicity, oxidative stress and genotoxicity induced by glass fibers on human alveolar epithelial cell line A549

2015 ◽  
Vol 29 (3) ◽  
pp. 551-557 ◽  
Author(s):  
Venerando Rapisarda ◽  
Carla Loreto ◽  
Caterina Ledda ◽  
Giuseppe Musumeci ◽  
Massimo Bracci ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
Cell Line ◽  
Alveolar Epithelial Cell ◽  
Glass Fibers ◽  
Epithelial Cell Line ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cell

scholarly journals Chemokine Production by a Human Alveolar Epithelial Cell Line in Response to Mycobacterium tuberculosis

1998 ◽  
Vol 66 (3) ◽  
pp. 1121-1126 ◽  
Author(s):  
Yuanguang Lin ◽  
Ming Zhang ◽  
Peter F. Barnes
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Epithelial Cell ◽  
Cell Line ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial Cells ◽  
Epithelial Cell Line ◽  
Intracellular Growth ◽  
Chemokine Production ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cell

ABSTRACT To investigate the role of chemokines during the initial local response to Mycobacterium tuberculosis in the human lung, we studied chemokine production by the human alveolar epithelial cell line A549 after infection with M. tuberculosis. M. tuberculosis-infected A549 cells produced mRNAs and protein for monocyte chemotactic protein-1 (MCP-1) and interleukin-8 (IL-8) but not mRNAs for macrophage inflammatory protein 1α (MIP-1α), MIP-1β, and RANTES. Chemokine production in response to M. tuberculosis was not dependent on production of tumor necrosis factor alpha, IL-1β, or IL-6. Two virulent clinical M. tuberculosis isolates, the virulent laboratory strain H37Rv, and the avirulent strain H37Ra elicited production of comparable concentrations of MCP-1 and IL-8, whereas killed M. tuberculosis and three Mycobacterium avium strains did not. The three virulent M. tuberculosis strains grew more rapidly than the avirulent M. tuberculosisstrain in the alveolar epithelial cell line, and the threeM. avium strains did not grow intracellularly. These findings suggest that intracellular growth is necessary for mycobacteria to elicit production of MCP-1 and IL-8 by alveolar epithelial cells but that virulence and the rate of intracellular growth do not correlate with chemokine production. Alveolar epithelial cells may contribute to the local inflammatory response in human tuberculosis by producing chemokines which attract monocytes, lymphocytes, and polymorphonuclear cells.

scholarly journals Inhibition Mir-92a Alleviates Oxidative Stress and Apoptosis of Alveolar Epithelial Cells Induced by Lipopolysaccharide Exposure through TLR2/AP-1 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Jian Cui ◽  
Huanhuan Ding ◽  
Yongyuan Yao ◽  
Wei Liu
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Lung Tissue ◽  
Cell Apoptosis ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial Cells ◽  
Rat Lung ◽  
Alveolar Epithelial

Objective. To probe into the role of miR-92a in alleviating oxidative stress and apoptosis of alveolar epithelial cell (AEC) injury induced by lipopolysaccharide (LPS) exposure through the Toll-like receptor (TLR) 2/activator protein-1 (AP-1) pathway. Methods. Acute lung injury (ALI) rat model and ALI alveolar epithelial cell model were constructed to inhibit the expression of miR-92a/TLR2/AP-1 in rat and alveolar epithelial cells (AECs), to detect the changes of oxidative stress, inflammatory response, and cell apoptosis in rat lung tissues and AECs, and to measure the changes of wet-dry weight (W/D) ratio in rat lung tissues. Results. Both inhibition of miR-92a expression and knockout of TLR2 and AP-1 gene could reduce LPS-induced rat ALI, alleviate pulmonary edema, inhibit oxidative stress and inflammatory response, and reduce apoptosis of lung tissue cells. In addition, the TLR2 and AP-1 levels in the lung tissues of ALI rats were noticed to be suppressed when inhibiting the expression of miR-92a, and the AP-1 level was also decreased after the knockout of TLR2 gene. Further, we verified this relationship in AECs and found that inhibition of miR-92a/TLR2/AP-1 also alleviated LPS-induced AEC injury, reduced cell apoptosis, and inhibited oxidative stress and inflammatory response. What is more, like that in rat lung tissue, the phenomenon also existed in AECs, that is, when the expression of miR-92a was inhibited, the expression of TLR2 and AP-1 was inhibited, and silencing TLR2 can reduce the expression level of AP-1. Conclusion. MiR-92a/TLR2/AP-1 is highly expressed in ALI, and its inhibition can improve oxidative stress and inflammatory response and reduce apoptosis of AECs.

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