scholarly journals 1α,25-dihydroxyvitamin D3 Attenuates TGF-β-Induced Pro-Fibrotic Effects in Human Lung Epithelial Cells through Inhibition of Epithelial–Mesenchymal Transition

Nutrients ◽  
2017 ◽  
Vol 9 (9) ◽  
pp. 980 ◽  
Author(s):  
Fei Jiang ◽  
Yong Yang ◽  
Lian Xue ◽  
Bingyan Li ◽  
Zengli Zhang
Keyword(s):  
Epithelial Cells ◽  
Human Lung ◽  
Epithelial Mesenchymal Transition ◽  
Lung Epithelial Cells ◽  
Dihydroxyvitamin D3 ◽  
Mesenchymal Transition ◽  
Lung Epithelial ◽  
Human Lung Epithelial Cells

scholarly journals TGF-β Induced CTGF Expression in Human Lung Epithelial Cells through ERK, ADAM17, RSK1, and C/EBPβ Pathways

2020 ◽  
Vol 21 (23) ◽  
pp. 9084
Author(s):  
Shu-Ching Ou ◽  
Kuan-Jen Bai ◽  
Wun-Hao Cheng ◽  
Jing-Yun Chen ◽  
Chien-Huang Lin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Human Lung ◽  
Tissue Growth ◽  
Lung Epithelial Cells ◽  
Mrna Levels ◽  
Mesenchymal Transition ◽  
Lung Epithelial ◽  
Human Lung Epithelial Cells

Background: Lung epithelial cells play critical roles in idiopathic pulmonary fibrosis. Methods: In the present study, we investigated whether transforming growth factor-β (TGF-β)-induced expression of connective tissue growth factor (CTGF) was regulated by the extracellular signal-regulated kinase (ERK)/a disintegrin and metalloproteinase 17 (ADAM17)/ribosomal S6 kinases 1 (RSK1)/CCAAT/enhancer-binding protein β (C/EBPβ) signaling pathway in human lung epithelial cells (A549). Results: Our results revealed that TGF-β-induced CTGF expression was weakened by ADAM17 small interfering RNA (ADAM17 siRNA), TNF-α processing inhibitor-0 (TAPI-0, an ADAM17 inhibitor), U0126 (an ERK inhibitor), RSK1 siRNA, and C/EBPβ siRNA. TGF-β-induced ERK phosphorylation as well as ADAM17 phosphorylation was attenuated by U0126. The TGF-β-induced increase in RSK1 phosphorylation was inhibited by TAPI-0 and U0126. TGF-β-induced C/EBPβ phosphorylation was weakened by U0126, ADAM17 siRNA, and RSK1 siRNA. In addition, TGF-β increased the recruitment of C/EBPβ to the CTGF promoter. Furthermore, TGF-β enhanced fibronectin (FN), an epithelial–mesenchymal transition (EMT) marker, and CTGF mRNA levels and reduced E-cadherin mRNA levels. Moreover, TGF-β-stimulated FN protein expression was reduced by ADAM17 siRNA and CTGF siRNA. Conclusion: The results suggested that TGF-β induces CTGF expression through the ERK/ADAM17/RSK1/C/EBPβ signaling pathway. Moreover, ADAM17 and CTGF participate in TGF-β-induced FN expression in human lung epithelial cells.

scholarly journals Concentration- and Time-Dependent Effects of Benzalkonium Chloride in Human Lung Epithelial Cells: Necrosis, Apoptosis, or Epithelial Mesenchymal Transition

Toxics ◽  
2020 ◽  
Vol 8 (1) ◽  
pp. 17 ◽  
Author(s):  
Sou Hyun Kim ◽  
Doyoung Kwon ◽  
Seunghyun Lee ◽  
Seung Won Son ◽  
Jung-Taek Kwon ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Benzalkonium Chloride ◽  
Human Lung ◽  
Epithelial Mesenchymal Transition ◽  
Membrane Damage ◽  
Lung Epithelial Cells ◽  
Time Dependent ◽  
Mesenchymal Transition ◽  
Cell Membrane Damage ◽  
Lung Epithelial

Benzalkonium chloride (BAC), an antimicrobial agent in inhalable medications and household sprays, has been reported to be toxic to pulmonary organs. Although cell membrane damage has been considered as the main cytotoxic mechanism of BAC, its concentration- and time-dependent cellular effects on lung epithelium have not been fully understood. In the present study, human lung epithelial (H358) cells were exposed to 0.2–40 μg/mL of BAC for 30 min or 21 days. Cell membranes were rapidly disrupted by 30 min exposure, but 24 h incubation of BAC (4–40 μg/mL) predominantly caused apoptosis rather than necrosis. BAC (2–4 μg/mL) induced mitochondrial depolarization, which may be associated with increased expression of pro-apoptotic proteins (caspase-3, PARP, Bax, p53, and p21), and decreased levels of the anti-apoptotic protein Bcl-2. The protein expression levels of IRE1α, BiP, CHOP, and p-JNK were also elevated by BAC (2–4 μg/mL) suggesting the possible involvement of endoplasmic reticulum stress in inducing apoptosis. Long-term (7–21 days) incubation with BAC (0.2–0.6 μg/mL) did not affect cell viability but led to epithelial-mesenchymal transition (EMT) as shown by the decrease of E-cadherin and the increase of N-cadherin, fibronectin, and vimentin, caused by the upregulation of EMT transcription factors, such as Snail, Slug, Twist1, Zeb1, and Zeb2. Therefore, we conclude that apoptosis could be an important mechanism of acute BAC cytotoxicity in lung epithelial cells, and chronic exposure to BAC even at sub-lethal doses can promote pulmonary EMT.

Legionella pneumophila induced microRNA expression in human lung epithelial cells

Pneumologie ◽  
2010 ◽  
Vol 64 (S 03) ◽  
Author(s):  
B Schmeck ◽  
B Dolniak ◽  
I Pollock ◽  
C Schulz ◽  
W Bertrams ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Legionella Pneumophila ◽  
Human Lung ◽  
Microrna Expression ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Human Lung Epithelial Cells
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