scholarly journals Inhibition of epidermal growth factor receptor attenuates atherosclerosis via decreasing inflammation and oxidative stress

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Lintao Wang ◽  
Zhouqing Huang ◽  
Weijian Huang ◽  
Xuemei Chen ◽  
Peiren Shan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Epidermal Growth ◽  
And Oxidative Stress

scholarly journals Oxidative Stress Causes Mucin Synthesis Via Transactivation of Epidermal Growth Factor Receptor: Role of Neutrophils

2000 ◽  
Vol 164 (3) ◽  
pp. 1546-1552 ◽  
Author(s):  
Kiyoshi Takeyama ◽  
Karim Dabbagh ◽  
Jae Jeong Shim ◽  
Trang Dao-Pick ◽  
Iris F. Ueki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Mucin Synthesis ◽  
Epidermal Growth

H2O2 mediates oxidative stress-induced epidermal growth factor receptor phosphorylation

2001 ◽  
Vol 122 (3) ◽  
pp. 205-214 ◽  
Author(s):  
Alexander Meves ◽  
Sibylle N. Stock ◽  
Astrid Beyerle ◽  
Mark R. Pittelkow ◽  
Dominik Peus
Keyword(s):  
Oxidative Stress ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Receptor Phosphorylation ◽  
Epidermal Growth

scholarly journals Triggering of Suicidal Erythrocyte Death by Gefitinib

2017 ◽  
Vol 41 (4) ◽  
pp. 1697-1708 ◽  
Author(s):  
Abdulla Al Mamun Bhuyan ◽  
Teresa Wagner ◽  
Hang Cao ◽  
Florian Lang
Keyword(s):  
Oxidative Stress ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Membrane ◽  
Kinase Inhibitor ◽  
Growth Factor Receptor ◽  
Annexin V ◽  
Forward Scatter ◽  
Epidermal Growth

Background/Aims: The epidermal growth factor receptor-tyrosine kinase inhibitor gefitinib is effective against several malignancies and is mainly utilized in the treatment of epidermal growth factor receptor mutation positive non-small cell lung cancer. The anti-cancer effect of the drug involves stimulation of apoptosis. Side effects of gefitinib include anemia. At least in theory, the development of anemia during gefitinib treatment could result from triggering of eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and by cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Signaling potentially stimulating eryptosis include increase of cytosolic Ca2+ activity ([Ca2+]i) and generation of oxidative stress. The present study explored, whether gefitinib stimulates eryptosis and, if so, whether its effect involves Ca2+ entry and/or oxidative stress. Methods: Flow cytometry was employed to quantify cell volume from forward scatter, phosphatidylserine exposure at the cell surface from annexin-V-binding, [Ca2+]i from Fluo3-fluorescence, and reactive oxygen species (ROS) abundance from 2’,7’-dichlorodihydrofluorescein diacetate (DCFDA) dependent fluorescence. Results: A 48 hours exposure of human erythrocytes to gefitinib (≥ 2 µg/ml) significantly decreased forward scatter and significantly increased the percentage of annexin-V-binding cells. Gefitinib did not significantly increase Fluo3-fluorescence but the effect of gefitinib on annexin-V-binding was significantly blunted by removal of extracellular Ca2+. Gefitinib further significantly increased DCFDA fluorescence. Conclusions: Gefitinib triggers erythrocyte shrinkage and phospholipid scrambling of the erythrocyte cell membrane, an effect at least in part dependent on extracellular Ca2+ and paralleled by oxidative stress.

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