BACKGROUND: Alveolar epithelial cell @entity204 plays a critical role in the pathogenesis of lipopolysaccharide (LPS)-induced @entity647 . Increased autophagy has a dual effect on cell survival. However, it is not known whether autophagy promotes @entity204 or survival in @entity1 alveolar epithelial cells exposed to LPS. METHODS: Genetic and pharmacological approaches were used to evaluate the effect of autophagy on A549 cell viability upon LPS exposure. The endoplasmic reticulum (ER) stress and unfolded protein response (UPR) pathways were examined with immunoblotting studies to further explore underlying mechanisms. RESULTS: Treatment with LPS (50   g/ml) led to autophagy activation and decreased cell viability in A549 cells. Blocking autophagy via short interfering RNA or inhibitor significantly decreased, whereas @entity3446 increased, the LPS-induced effect on viability. ER stress was activated in LPS-stimulated A549 cells, and ER stress inhibitor reduced LPS-induced autophagy. LPS activated only the @entity7952 pathway and had rarely effect on the @entity14920 and @entity5593 branches of the UPR in A549 cells. Moreover, the knockdown of @entity7952 and @entity15205 attenuated LPS-induced autophagy and promoted cell survival. CONCLUSION: In @entity1 alveolar epithelial A549 cells, LPS induces autophagic cell @entity204 that depends on the activation of the @entity7952 branch of the UPR upon ER stress.

Lipopolysaccharide Induces Autophagic Cell Death through the XXXX -Dependent Branch of the Unfolded Protein Response in @entity1 Alveolar Epithelial A549 Cells.

@entity1 :: ('9606', 'Species') :: ['human'] @entity15205 :: ('468', 'Gene') :: ['ATF4'] @entity7952 :: ('9451', 'Gene') :: ['PERK'] @entity3446 :: ('MESH:D020123', 'Chemical') :: ['rapamycin'] @entity14920 :: ('22926', 'Gene') :: ['ATF6'] @entity204 :: ('MESH:D003643', 'Disease') :: ['death'] @entity5593 :: ('2081', 'Gene') :: ['IRE1'] @entity647 :: ('MESH:D055371', 'Disease') :: ['acute lung injury']
@entity7952 :: (9451,Gene) :: ['PERK']
