40 OVEREXPRESSION OF ANTIOXIDANT ENZYMES IN LUNG EPITHELIAL CELLS PREVENTS DAMAGE FROM AIRBORNE PARTICULATE MATTER-INDUCED OXIDANT INJURY.: TABLE 1

2006 ◽  
Vol 54 (2) ◽  
pp. S350.1-S350
Author(s):  
S. Soberanes ◽  
V. Panduri ◽  
H. Wang ◽  
G. Mutlu ◽  
G. R. Budinger ◽  
...  
Keyword(s):  
Antioxidant Enzymes ◽  
Particulate Matter ◽  
Epithelial Cells ◽  
Airborne Particulate Matter ◽  
Lung Epithelial Cells ◽  
Airborne Particulate ◽  
Oxidant Injury ◽  
Lung Epithelial

scholarly journals Airborne Particulate Matter (PM10) Inhibits Apoptosis through PI3K/AKT/FoxO3a Pathway in Lung Epithelial Cells: The Role of a Second Oxidant Stimulus

2020 ◽  
Vol 21 (2) ◽  
pp. 473 ◽  
Author(s):  
Claudia M. García-Cuellar ◽  
Yolanda I. Chirino ◽  
Rocío Morales-Bárcenas ◽  
Ernesto Soto-Reyes ◽  
Raúl Quintana-Belmares ◽  
...  
Keyword(s):  
Particulate Matter ◽  
A549 Cells ◽  
Airborne Particulate Matter ◽  
Lung Epithelial Cells ◽  
Airborne Particulate ◽  
Cellular Survival ◽  
Lung Epithelial ◽  
Pm10 Exposure ◽  
Phosphorylation Rate

Outdoor particulate matter (PM10) exposure is carcinogenic to humans. The cellular mechanism by which PM10 is associated specifically with lung cancer includes oxidative stress and damage to proteins, lipids, and DNA in the absence of apoptosis, suggesting that PM10 induces cellular survival. We aimed to evaluate the PI3K/AKT/FoxO3a pathway as a mechanism of cell survival in lung epithelial A549 cells exposed to PM10 that were subsequently challenged with hydrogen peroxide (H2O2). Our results showed that pre-exposure to PM10 followed by H2O2, as a second oxidant stimulus increased the phosphorylation rate of pAKTSer473, pAKTThr308, and pFoxO3aSer253 2.5-fold, 1.8-fold, and 1.2-fold, respectively. Levels of catalase and p27kip1, which are targets of the PIK3/AKT/FoxO3a pathway, decreased 38.1% and 62.7%, respectively. None of these changes had an influence on apoptosis; however, the inhibition of PI3K using the LY294002 compound revealed that the PI3K/AKT/FoxO3a pathway was involved in apoptosis evasion. We conclude that nontoxic PM10 exposure predisposes lung epithelial cell cultures to evade apoptosis through the PI3K/AKT/FoxO3a pathway when cells are treated with a second oxidant stimulus.

Sign in / Sign up

Export Citation Format

Share Document