title: SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation.
abstract: Chronic obstructive pulmonary disease (COPD), a major global health problem with increasing morbidity and mortality rates, is anticipated to become the third leading cause of death worldwide by 2020. COPD arises from exposure to cigarette smoke. Acrolein, which is contained in cigarette smoke, is the most important risk factor for COPD. It causes lung injury through altering apoptosis and causes inflammation by augmenting p53 phosphorylation and producing reactive oxygen species (ROS). Secretoglobin (SCGB) 3A2, a secretory protein predominantly present in the epithelial cells of the lungs and trachea, is a cytokine-like small molecule having anti-inflammatory, antifibrotic, and growth factor activities. In this study, the effect of SCGB3A2 on acrolein-related apoptosis was investigated using the mouse fibroblast cell line MLg as the first step in determining the possible therapeutic value of SCGB3A2 in COPD. Acrolein increased the production of ROS and phosphorylation of p53 and induced apoptosis in MLg cells. While the extent of ROS production induced by acrolein was not affected by SCGB3A2, p53 phosphorylation was significantly decreased by SCGB3A2. These results demonstrate that SCGB3A2 inhibited acrolein-induced apoptosis through decreased p53 phosphorylation, not altered ROS levels.
authors.affiliation: Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University , Yonezawa, Yamagata 992-8510, Japan.
authors.forename: Reiko
authors.initials: R
authors.lastname: Kurotani
authors.affiliation: Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University , Yonezawa, Yamagata 992-8510, Japan.
authors.forename: Reika
authors.initials: R
authors.lastname: Shima
authors.affiliation: Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University , Yonezawa, Yamagata 992-8510, Japan.
authors.forename: Yuki
authors.initials: Y
authors.lastname: Miyano
authors.affiliation: Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University , Yonezawa, Yamagata 992-8510, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Sakahara
authors.affiliation: Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University , Yonezawa, Yamagata 992-8510, Japan.
authors.forename: Yoshie
authors.initials: Y
authors.lastname: Matsumoto
authors.affiliation: Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine , 2-2-2 Iida-Nishi, Yamagata 990-9585, Japan.
authors.forename: Yoko
authors.initials: Y
authors.lastname: Shibata
authors.affiliation: Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University , Yonezawa, Yamagata 992-8510, Japan.
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Abe
authors.affiliation: Laboratory of Metabolism, National Cancer Institute, National Institutes of Health , Bethesda, MD 20892.
authors.forename: Shioko
authors.initials: S
authors.lastname: Kimura
keywords: acrolein; apoptosis; chronic obstructive pulmonary disease (COPD); p53; secretoglobin (SCGB) 3A2