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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 170309, 15 pages
Research Article

Enhancement of the Acrolein-Induced Production of Reactive Oxygen Species and Lung Injury by GADD34

1Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan
2Department of Immunology, Norman Bethune College of Medicine, Jilin University, Changchun 130021, China

Received 26 November 2014; Revised 28 January 2015; Accepted 28 January 2015

Academic Editor: Sidhartha D. Ray

Copyright © 2015 Yang Sun et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Chronic obstructive pulmonary disease (COPD) is characterized by lung destruction and inflammation. As a major compound of cigarette smoke, acrolein plays a critical role in the induction of respiratory diseases. GADD34 is known as a growth arrest and DNA damage-related gene, which can be overexpressed in adverse environmental conditions. Here we investigated the effects of GADD34 on acrolein-induced lung injury. The intranasal exposure of acrolein induced the expression of GADD34, developing the pulmonary damage with inflammation and increase of reactive oxygen species (ROS). Conversely, the integrality of pulmonary structure was preserved and the generation of ROS was reduced in GADD34-knockout mice. Acrolein-induced phosphorylation of eIF2α in GADD34-knockout epithelial cells by shRNA protected cell death by reducing misfolded protein-caused oxidative stress. These data indicate that GADD34 participates in the development of acrolein-induced lung injury.