Cigarette smoke extract increases mitochondrial membrane permeability through activation of adenine nucleotide translocator (ANT) in lung epithelial cells

2020 ◽  
Vol 525 (3) ◽  
pp. 733-739 ◽  
Author(s):  
Kaiyue Wu ◽  
Guangxin Luan ◽  
Yanhong Xu ◽  
Shuang Shen ◽  
Shengnan Qian ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Membrane Permeability ◽  
Cigarette Smoke ◽  
Mitochondrial Membrane ◽  
Adenine Nucleotide ◽  
Cigarette Smoke Extract ◽  
Lung Epithelial Cells ◽  
Adenine Nucleotide Translocator ◽  
Mitochondrial Membrane Permeability ◽  
Lung Epithelial

Characterization of Cigarette Smoke Extract (CSE)-induced Cell Death in Lung Epithelial Cells

2005 ◽  
Vol 58 (1) ◽  
pp. 43
Author(s):  
Eun Kyung Choi ◽  
Yun Seup Kim ◽  
Jae Seuk Park ◽  
Young Koo Jee ◽  
Kye Young Lee
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

scholarly journals Conditioned Media of Adipose-Derived Stem Cells Suppresses Sidestream Cigarette Smoke Extract Induced Cell Death and Epithelial-Mesenchymal Transition in Lung Epithelial Cells

2021 ◽  
Vol 22 (21) ◽  
pp. 12069
Author(s):  
Tzu-Yin Chen ◽  
Chia-Hao Liu ◽  
Tsung-Hsien Chen ◽  
Mei-Ru Chen ◽  
Shan-Wen Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Epithelial Mesenchymal Transition ◽  
Cigarette Smoke Extract ◽  
Lung Epithelial Cells ◽  
Second Hand Smoke ◽  
Mesenchymal Transition ◽  
Lung Epithelial ◽  
Tgf Β1

The role of the epithelial–mesenchymal transition (EMT) in lung epithelial cells is increasingly being recognized as a key stage in the development of COPD, fibrosis, and lung cancers, which are all highly associated with cigarette smoking and with exposure to second-hand smoke. Using the exposure of human lung cancer epithelial A549 cells and non-cancerous Beas-2B cells to sidestream cigarette smoke extract (CSE) as a model, we studied the protective effects of adipose-derived stem cell-conditioned medium (ADSC-CM) against CSE-induced cell death and EMT. CSE dose-dependently induced cell death, decreased epithelial markers, and increased the expression of mesenchymal markers. Upstream regulator analysis of differentially expressed genes after CSE exposure revealed similar pathways as those observed in typical EMT induced by TGF-β1. CSE-induced cell death was clearly attenuated by ADSC-CM but not by other control media, such as a pass-through fraction of ADSC-CM or A549-CM. ADSC-CM effectively inhibited CSE-induced EMT and was able to reverse the gradual loss of epithelial marker expression associated with TGF-β1 treatment. CSE or TGF-β1 enhanced the speed of A549 migration by 2- to 3-fold, and ADSC-CM was effective in blocking the cell migration induced by either agent. Future work will build on the results of this in vitro study by defining the molecular mechanisms through which ADSC-CM protects lung epithelial cells from EMT induced by toxicants in second-hand smoke.

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