SGK1 inhibits PM2.5-induced apoptosis and oxidative stress in human lung alveolar epithelial A549 cells

Jin Li; Qiulian Zhou; Tingting Yang; Yongqin Li; Yuhui Zhang; Jinhua Wang; Zheng Jiao

doi:10.1016/j.bbrc.2018.02.002

SGK1 inhibits PM2.5-induced apoptosis and oxidative stress in human lung alveolar epithelial A549 cells

Biochem Biophys Res Commun. 2018 Feb 19;496(4):1291-1295. doi: 10.1016/j.bbrc.2018.02.002. Epub 2018 Feb 3.

Authors

Jin Li¹, Qiulian Zhou¹, Tingting Yang², Yongqin Li², Yuhui Zhang³, Jinhua Wang⁴, Zheng Jiao⁵

Affiliations

¹ Shanghai Applied Radiation Institute, School of Environmental and Chemical Engineering, Shanghai University, Shanghai, China; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai, China.
² Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai, China.
³ State Key Laboratory of Cardiovascular Disease, Heart Failure Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
⁴ Shanghai Applied Radiation Institute, School of Environmental and Chemical Engineering, Shanghai University, Shanghai, China. Electronic address: jinhuawang@staff.shu.edu.cn.
⁵ Shanghai Applied Radiation Institute, School of Environmental and Chemical Engineering, Shanghai University, Shanghai, China. Electronic address: zjiao@shu.edu.cn.

PMID: 29412164
DOI: 10.1016/j.bbrc.2018.02.002

Abstract

Emerging evidence demonstrated that particulate matter 2.5 (PM2.5) is an important environmental risk factor for lung diseases. Serum- and glucocorticoid-inducible kinase 1(SGK1) was reported to be a crucial factor for cell survival. However, the role of SGK1 in PM2.5-induced cell injury is still unclear. In this work, we firstly found that the expression of SGK1 was decreased in PM2.5-treated human lung alveolar epithelial (A549) cells by western blot. In addition, overexpression of SGK1 significantly attenuated A549 cell apoptosis and reduced the reactive oxygen species (ROS) generation induced by PM2.5. Moreover, we found that PM2.5 exposure significantly promoted the ERK1/2 activation and inhibited the AKT activation, whereas overexpression of SGK1 could reverse that. Finally, the results of the rescue experiment showed that MK2206 (AKT inhibitor) could rescue the impact of SGK1 on A549 cell apoptosis, while PD98059 (ERK1/2 inhibitor) could not further aggravate the impact. Taken together, our results suggest that SGK1 inhibits PM2.5-induced cell apoptosis and ROS generation via ERK1/2 and AKT signaling pathway in human lung alveolar epithelial A549 cells.

Keywords: Cell apoptosis; PM2.5; ROS production; SGK1.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

A549 Cells
Alveolar Epithelial Cells / cytology*
Alveolar Epithelial Cells / drug effects
Alveolar Epithelial Cells / physiology*
Apoptosis / drug effects
Apoptosis / physiology*
Humans
Immediate-Early Proteins / metabolism*
MAP Kinase Signaling System / drug effects
MAP Kinase Signaling System / physiology
Oxidative Stress / drug effects
Oxidative Stress / physiology*
Particulate Matter / administration & dosage*
Protein Serine-Threonine Kinases / metabolism*
Reactive Oxygen Species / metabolism*

Substances

Immediate-Early Proteins
Particulate Matter
Reactive Oxygen Species
Protein Serine-Threonine Kinases
serum-glucocorticoid regulated kinase