TDAG51 deficiency promotes oxidative stress-induced apoptosis through the generation of reactive oxygen species in mouse embryonic fibroblasts.
- Author:
Eui Soon PARK
1
;
Juhyeok KIM
;
Tae Uk HA
;
Jong Soon CHOI
;
Kwan Soo HONG
;
Jaerang RHO
Author Information
1. Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, Korea. jrrho@cnu.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
apoptosis;
oxidative stress;
ROS;
TDAG51
- MeSH:
Animals;
*Apoptosis;
Embryo, Mammalian/*cytology;
Fibroblasts/enzymology/*metabolism/pathology;
Gene Expression Regulation;
Intracellular Space/metabolism;
Mice;
Mitogen-Activated Protein Kinases/metabolism;
NF-kappa B/metabolism;
*Oxidative Stress/genetics;
Reactive Oxygen Species/*metabolism;
Signal Transduction;
Transcription Factors/*deficiency/genetics/metabolism
- From:Experimental & Molecular Medicine
2013;45(8):e35-
- CountryRepublic of Korea
- Language:English
-
Abstract:
Apoptosis has an important role in maintaining tissue homeostasis in cellular stress responses such as inflammation, endoplasmic reticulum stress, and oxidative stress. T-cell death-associated gene 51 (TDAG51) is a member of the pleckstrin homology-like domain family and was first identified as a pro-apoptotic gene in T-cell receptor-mediated cell death. However, its pro-apoptotic function remains controversial. In this study, we investigated the role of TDAG51 in oxidative stress-induced apoptotic cell death in mouse embryonic fibroblasts (MEFs). TDAG51 expression was highly increased by oxidative stress responses. In response to oxidative stress, the production of intracellular reactive oxygen species was significantly enhanced in TDAG51-deficient MEFs, resulting in the activation of caspase-3. Thus, TDAG51 deficiency promotes apoptotic cell death in MEFs, and these results indicate that TDAG51 has a protective role in oxidative stress-induced cell death in MEFs.
