SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation

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 th...

Full description

Bibliographic Details
Main Authors:	Kurotani, Reiko, Shima, Reika, Miyano, Yuki, Sakahara, Satoshi, Matsumoto, Yoshie, Shibata, Yoko, Abe, Hiroyuki, Kimura, Shioko
Format:	Online
Language:	English
Published:	JAPAN SOCIETY OF HISTOCHEMISTRY AND CYTOCHEMISTRY 2015
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4427566/

id	pubmed-4427566
recordtype	oai_dc
spelling	pubmed-44275662015-05-27 SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation Kurotani, Reiko Shima, Reika Miyano, Yuki Sakahara, Satoshi Matsumoto, Yoshie Shibata, Yoko Abe, Hiroyuki Kimura, Shioko Regular Article 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. JAPAN SOCIETY OF HISTOCHEMISTRY AND CYTOCHEMISTRY 2015-04-28 2015-04-24 /pmc/articles/PMC4427566/ /pubmed/26019375 http://dx.doi.org/10.1267/ahc.14065 Text en 2015 The Japan Society of Histochemistry and Cytochemistry This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Kurotani, Reiko Shima, Reika Miyano, Yuki Sakahara, Satoshi Matsumoto, Yoshie Shibata, Yoko Abe, Hiroyuki Kimura, Shioko
spellingShingle	Kurotani, Reiko Shima, Reika Miyano, Yuki Sakahara, Satoshi Matsumoto, Yoshie Shibata, Yoko Abe, Hiroyuki Kimura, Shioko SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation
author_facet	Kurotani, Reiko Shima, Reika Miyano, Yuki Sakahara, Satoshi Matsumoto, Yoshie Shibata, Yoko Abe, Hiroyuki Kimura, Shioko
author_sort	Kurotani, Reiko
title	SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation
title_short	SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation
title_full	SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation
title_fullStr	SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation
title_full_unstemmed	SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation
title_sort	scgb3a2 inhibits acrolein-induced apoptosis through decreased p53 phosphorylation
description	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.
publisher	JAPAN SOCIETY OF HISTOCHEMISTRY AND CYTOCHEMISTRY
publishDate	2015
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4427566/
_version_	1613221940695138304

SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation

Similar Items