Airborne particulate matter (PM10) inhibits apoptosis through PI3K/AKT/FoxO3a pathway in lung epithelial cells: the role of a second oxidant stimulus.

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 aim...

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Bibliographic Details
Authors: CLAUDIA MARIA GARCIA CUELLAR, YOLANDA IRASEMA CHIRINO LOPEZ, MARIA DEL ROCIO MORALES BARCENAS, ERNESTO SOTO REYES SOLIS, RAUL OMAR QUINTANA BELMARES, MIGUEL SANTIBAÑEZ ANDRADE, YESENNIA SANCHEZ PEREZ
Format: article
Status:Published version
Publication Date:2020
Country:México
Institution:Universidad Autónoma Metropolitana
Repository:Concentración de Recursos de Información Científica y Académica, UAM Cuajimalpa
Language:English
OAI Identifier:oai:ilitia.cua.uam.mx:123456789/907
Online Access:http://ilitia.cua.uam.mx:8080/jspui/handle/123456789/907
Access Level:Open access
Keyword:info:eu-repo/classification/cti/2
Materia particular
Vía PI3K / AKT / FoxO3A
Apoptosis
Description
Summary: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.

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