Exp Mol Med.  2013 Aug;45(8):e35.

TDAG51 deficiency promotes oxidative stress-induced apoptosis through the generation of reactive oxygen species in mouse embryonic fibroblasts

• Park ES
• Kim J
• Ha TU
• Choi JS
• Hong KS
• Rho J

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.

Keyword

apoptosis; oxidative stress; ROS; TDAG51

MeSH Terms

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
NF-kappa B
Reactive Oxygen Species
Transcription Factors
Mitogen-Activated Protein Kinases