Perilipin 5 Protects against Cellular Oxidative Stress by Enhancing Mitochondrial Function in HepG2 Cells

Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide. Reactive oxygen species (ROS), as potent oxidants in cells, have been shown to promote the development of NAFLD. Previous studies reported that for ROS-induced cellular oxidative stress, promoting lipid dro...

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Published inCells (Basel, Switzerland) Vol. 8; no. 10; p. 1241
Main Authors Tan, Yanjie, Jin, Yi, Wang, Qian, Huang, Jin, Wu, Xiang, Ren, Zhuqing
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 11.10.2019
MDPI
Subjects
Antioxidants
Binding sites
Cytochrome
Enzymes
Fatty acids
Fatty liver
Gene expression
Hepatitis
Hepatocytes
Hydrogen peroxide
lipid droplet
Lipids
Lipopolysaccharides
Liver cancer
Liver diseases
Localization
Mitochondria
mRNA
Musculoskeletal system
Oxidants
Oxidation
Oxidative stress
perilipin 5
Proteins
Reactive oxygen species
ros
Stem cells
lipid droplet
mitochondria
ROS
perilipin 5
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Summary:Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide. Reactive oxygen species (ROS), as potent oxidants in cells, have been shown to promote the development of NAFLD. Previous studies reported that for ROS-induced cellular oxidative stress, promoting lipid droplet (LD) accumulation is associated with the cellular antioxidation process. However, the regulatory role of LDs in relieving cellular oxidative stress is poorly understood. Here, we showed that ( ), a key LD protein related to mitochondria-LD contact, reduced ROS levels and improved mitochondrial function in HepG2 cells. Both mRNA and protein levels of were significantly increased in cells with hydrogen peroxide or lipopolysaccharide (LPS) treatment ( < 0.05). Additionally, the overexpression of promoted LD formation and mitochondria-LD contact, reduced cellular ROS levels and up-regulated mitochondrial function-related genes such as and . Knockdown , meanwhile, showed opposite effects. Furthermore, we identified that cellular oxidative stress up-regulated expression via the JNK-p38-ATF pathway. This study shows that the up-regulation of is a kind of survival strategy for cells in response to stress. can be a potential therapeutic target in NAFLD.
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These two authors contributed equally to this work.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells8101241