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RRC ID 67745
著者 Sun Y, Ito S, Nishio N, Tanaka Y, Chen N, Liu L, Isobe K.
タイトル Enhancement of the acrolein-induced production of reactive oxygen species and lung injury by GADD34.
ジャーナル Oxid Med Cell Longev
Abstract 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.
巻・号 2015
ページ 170309
公開日 2015-1-1
DOI 10.1155/2015/170309
PMID 25821552
PMC PMC4364366
MeSH Acetylcysteine / pharmacology Acrolein / toxicity* Animals Apoptosis / drug effects Cells, Cultured Endoplasmic Reticulum Stress / drug effects Epithelial Cells / cytology Epithelial Cells / metabolism Female Inflammation Lung / drug effects Lung / metabolism Lung / pathology Lung Injury / chemically induced* Lung Injury / metabolism Lung Injury / pathology Mice Mice, Inbred C57BL Mice, Knockout Phosphorylation Protein Phosphatase 1 / antagonists & inhibitors Protein Phosphatase 1 / genetics Protein Phosphatase 1 / metabolism* Protein Serine-Threonine Kinases / metabolism RNA Interference RNA, Small Interfering / metabolism Reactive Oxygen Species / metabolism*
IF 5.076
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