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 ◽  
...  
2001 ◽  
Vol 25 (4) ◽  
pp. 507-514 ◽  
Author(s):  
Elodie Nabeyrat ◽  
Sophie Corroyer ◽  
Valérie Besnard ◽  
Véronique Cazals-Laville ◽  
Jacques Bourbon ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Jian Cui ◽  
Hailin Zhao ◽  
Chunyan Wang ◽  
James J. Sun ◽  
Kaizhi Lu ◽  
...  

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.


Head & Neck ◽  
2012 ◽  
Vol 35 (9) ◽  
pp. 1295-1302 ◽  
Author(s):  
Mei-Chi Chang ◽  
Chiu-Po Chan ◽  
Wei-Ting Wang ◽  
Bei-En Chang ◽  
Jang-Jaer Lee ◽  
...  

2004 ◽  
Vol 91 (10) ◽  
pp. 1842-1850 ◽  
Author(s):  
M Scaltriti ◽  
S Bettuzzi ◽  
R M Sharrard ◽  
A Caporali ◽  
A E Caccamo ◽  
...  

2006 ◽  
Vol 290 (6) ◽  
pp. L1216-L1226 ◽  
Author(s):  
Somshuvra Mukhopadhyay ◽  
Pravin B. Sehgal

Monocrotaline (MCT) causes pulmonary hypertension in the rat by a mechanism characterized by megalocytosis (enlarged cells with enlarged endoplasmic reticulum and Golgi and a cell cycle arrest) of pulmonary arterial endothelial (PAEC), arterial smooth muscle, and type II alveolar epithelial cells. In cell culture, although megalocytosis is associated with a block in entry into mitosis in both lung endothelial and epithelial cells, DNA synthesis is stimulated in endothelial but inhibited in epithelial cells. The molecular mechanism(s) for this dichotomy are unclear. While MCTP-treated PAEC and lung epithelial (A549) cells both showed an increase in the “promitogenic” transcription factor STAT3 levels and in the IL-6-induced nuclear pool of PY-STAT3, this was transcriptionally inactive in A549 but not in PAEC cells. This lack of transcriptional activity of STAT3 in A549 cells correlated with the cytoplasmic sequestration of the STAT3 coactivators CBP/p300 and SRC1/NcoA in A549 cells but not in PAEC. Both cell types displayed a Golgi trafficking block, loss of caveolin-1 rafts, and increased nuclear Ire1α, but an incomplete unfolded protein response (UPR) with little change in levels of UPR-induced chaperones including GRP78/BiP. There were discordant alterations in cell cycle regulatory proteins in the two cell types such as increase in levels of both cyclin D1 and p21 simultaneously, but with a decrease in cdc2/cdk1, a kinase required for entry into mitosis. While both cell types showed increased cytoplasmic geminin, the DNA synthesis-initiating protein Cdt1 was predominantly nuclear in PAEC but remained cytoplasmic in A549 cells, consistent with the stimulation of DNA synthesis in the former but an inhibition in the latter cell type. Thus differences in cell type-specific alterations in subcellular trafficking of critical regulatory molecules (such as CBP/p300, SRC1/NcoA, Cdt1) likely account for the dichotomy of the effects of MCTP on DNA synthesis in endothelial and epithelial cells.


Sign in / Sign up

Export Citation Format

Share Document