Peroxiredoxin I regulates the component expression of gamma-secretase complex causing the Alzheimer's disease.
10.5625/lar.2011.27.4.293
- Author:
Young Ju LEE
1
;
Jun Seo GOO
;
Ji Eun KIM
;
So Hee NAM
;
In Sik HWANG
;
Sun Il CHOI
;
Hye Ryun LEE
;
Eon Phil LEE
;
Hae Wook CHOI
;
Hong Sung KIM
;
Jae Ho LEE
;
Young Jin JUNG
;
Hak Jin KIM
;
Dae Youn HWANG
Author Information
1. Department of Biomaterials Science, College of Natural Resources and Life Science, Pusan National University, Miryang, Korea. dyhwang@pusan.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Peroxiredoxin I;
gamma-secretase complex;
Alzheimer's disease;
Abeta-42 peptides
- MeSH:
Alzheimer Disease;
Amyloid Precursor Protein Secretases;
Animals;
Brain;
Hippocampus;
Humans;
Mice;
Models, Animal;
Neuroblastoma;
Peptides;
Peroxiredoxins;
RNA, Messenger;
Signal Transduction
- From:Laboratory Animal Research
2011;27(4):293-299
- CountryRepublic of Korea
- Language:English
-
Abstract:
Peroxiredoxin I (Prx I) is a member of the peroxiredoxins (Prxs) family, which are antioxidant enzymes that regulate various cellular process via intracellular oxidative signal pathways. In order to investigate the correlation between Prx I and the gamma-secretase complex, which causes Alzheimer's disease (AD), the expression level of Prx I was firstly evaluated in an animal model for AD. NSE/hPen-2 transgenic (Tg) mice, which were used as animal model in this study, showed a high level of Pen-2 expression and accumulation of Abeta-42 peptides in the hippocampus of brain. The expression level of Prx I was significantly higher on the mRNA and protein level in the brain of this model, while not change in Prx VI expression was observed. Furthermore, to verify the effect of Prx I on the gamma-secretase components in vitro, the expression level of these components was analyzed in the Prx I transfectants. Of the components of the gamma-secretase complex, the expression of PS-2 and Pen-2 was lower in the transfectants overexpressing Prx I compared to the vector transfectants. However, the expression of APP, NCT and APH-1 did not change in Prx I transfectants. Therefore, these results suggested that the expression of Prx I may be induced by the accumulation of Abeta-42 peptides and the overexpression of Prx I in neuroblastoma cells may regulate the expression of gamma-secretase components.
