scholarly journals Acute Effects of Cigarette Smoke Extract on Alveolar Epithelial Sodium Channel Activity and Lung Fluid Clearance

2013 ◽  
Vol 49 (2) ◽  
pp. 251-259 ◽  
Author(s):  
Charles A. Downs ◽  
Lisa H. Kreiner ◽  
David Q. Trac ◽  
My N. Helms
Keyword(s):  
Sodium Channel ◽  
Cigarette Smoke ◽  
Epithelial Sodium Channel ◽  
Cigarette Smoke Extract ◽  
Channel Activity ◽  
Acute Effects ◽  
Alveolar Epithelial ◽  
Lung Fluid

Alveolar epithelial cells type II show a high sensitivity to cigarette smoke extract

Pneumologie ◽  
2014 ◽  
Vol 68 (06) ◽  
Author(s):  
S Seehase ◽  
B Baron-Luehr ◽  
C Kugler ◽  
E Vollmer ◽  
T Goldmann
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
High Sensitivity ◽  
Cigarette Smoke Extract ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Alveolar Epithelial

scholarly journals MicroRNA 16 modulates epithelial sodium channel in human alveolar epithelial cells

2012 ◽  
Vol 426 (2) ◽  
pp. 203-208 ◽  
Author(s):  
Prasanna Tamarapu Parthasarathy ◽  
Lakshmi Galam ◽  
Bao Huynh ◽  
Asfiya Yunus ◽  
Toaa Abuelenen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cells

Cigarette smoke extract affects mitochondrial function in alveolar epithelial cells

2014 ◽  
Vol 307 (11) ◽  
pp. L895-L907 ◽  
Author(s):  
Korbinian Ballweg ◽  
Kathrin Mutze ◽  
Melanie Königshoff ◽  
Oliver Eickelberg ◽  
Silke Meiners
Keyword(s):  
Stress Response ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Cellular Stress ◽  
Cigarette Smoke Extract ◽  
Mitochondrial Fusion ◽  
Alveolar Epithelial Cells ◽  
Mitochondrial Morphology ◽  
Mild Stress ◽  
Alveolar Epithelial

Cigarette smoke is the main risk factor for chronic obstructive pulmonary disease (COPD). Exposure of cells to cigarette smoke induces an initial adaptive cellular stress response involving increased oxidative stress and induction of inflammatory signaling pathways. Exposure of mitochondria to cellular stress alters their fusion/fission dynamics. Whereas mild stress induces a prosurvival response termed stress-induced mitochondrial hyperfusion, severe stress results in mitochondrial fragmentation and mitophagy. In the present study, we analyzed the mitochondrial response to mild and nontoxic doses of cigarette smoke extract (CSE) in alveolar epithelial cells. We characterized mitochondrial morphology, expression of mitochondrial fusion and fission genes, markers of mitochondrial proteostasis, as well as mitochondrial functions such as membrane potential and oxygen consumption. Murine lung epithelial (MLE)12 and primary mouse alveolar epithelial cells revealed pronounced mitochondrial hyperfusion upon treatment with CSE, accompanied by increased expression of the mitochondrial fusion protein mitofusin 2 and increased metabolic activity. We did not observe any alterations in mitochondrial proteostasis, i.e., induction of the mitochondrial unfolded protein response or mitophagy. Therefore, our data indicate an adaptive prosurvival response of mitochondria of alveolar epithelial cells to nontoxic concentrations of CSE. A hyperfused mitochondrial network, however, renders the cell more vulnerable to additional stress, such as sustained cigarette smoke exposure. As such, cigarette smoke-induced mitochondrial hyperfusion, although part of a beneficial adaptive stress response in the first place, may contribute to the pathogenesis of COPD.

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