SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation

• Kurotani Reiko

  Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University

• Shima Reika

  Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University

• Miyano Yuki

  Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University

• Sakahara Satoshi

  Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University

• Matsumoto Yoshie

  Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University

• Shibata Yoko

  Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine

• Abe Hiroyuki

  Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University

• Kimura Shioko

  Laboratory of Metabolism, National Cancer Institute, National Institutes ‍of Health

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.

Journal

• ACTA HISTOCHEMICA ET CYTOCHEMICA

  ACTA HISTOCHEMICA ET CYTOCHEMICA 48 (2), 61-68, 2015

  JAPAN SOCIETY OF HISTOCHEMISTRY AND CYTOCHEMISTRY

Keywords

• secretoglobin (SCGB) 3A2
• chronic obstructive pulmonary disease (COPD)
• apoptosis
• acrolein
• p53

Details

• CRID: 1390282679837967104
• NII Article ID: 130005068296
• DOI: 10.1267/ahc.14065
• ISSN: 13475800
• ISSN: 00445991
• Web Site: https://www.jstage.jst.go.jp/article/ahc/48/2/48_14065/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2016078186
• Text Lang: en
• Data Source:
  • JaLC
  • Crossref
  • CiNii Articles
  • KAKEN
• Abstract License Flag: Disallowed