Cigarette smoke induces endoplasmic reticulum stress response and proteasomal dysfunction in human alveolar epithelial cells

2012 ◽  
Vol 98 (1) ◽  
pp. 316-325 ◽  
Author(s):  
Anita Somborac-Bačura ◽  
Marco van der Toorn ◽  
Lorenza Franciosi ◽  
Dirk-Jan Slebos ◽  
Tihana Žanić-Grubišić ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Stress Response ◽  
Epithelial Cells ◽  
Endoplasmic Reticulum Stress ◽  
Cigarette Smoke ◽  
Alveolar Epithelial Cells ◽  
Endoplasmic Reticulum Stress Response ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cells

scholarly journals Alveolar epithelial cells undergo epithelial-to-mesenchymal transition in response to endoplasmic reticulum stress.

2015 ◽  
Vol 290 (6) ◽  
pp. 3277-3277 ◽  
Author(s):  
Harikrishna Tanjore ◽  
Dong-Sheng Cheng ◽  
Amber L. Degryse ◽  
Donald F. Zoz ◽  
Rasul Abdolrasulnia ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Epithelial Cells ◽  
Endoplasmic Reticulum Stress ◽  
Epithelial To Mesenchymal Transition ◽  
Alveolar Epithelial Cells ◽  
Mesenchymal Transition ◽  
Alveolar Epithelial

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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