Mercury induced the Accumulation of Amyloid Beta (Abeta) in PC12 Cells: The Role of Production and Degradation of Abeta.
- Author:
Ji Won SONG
1
;
Byung Sun CHOI
Author Information
1. Department of Preventive Medicine, College of Medicine, Chung-Ang University, Seoul, Korea. bschoi@cau.ac.kr
- Publication Type:Original Article
- Keywords:
Alzheimer's disease;
Amyloid beta;
Mercury;
Amyloid precursor protein;
beta-Secretase;
Neprilysin
- MeSH:
Aluminum;
Alzheimer Disease;
Amyloid beta-Peptides;
Amyloid Precursor Protein Secretases;
Amyloid*;
Animals;
Brain;
Copper;
Mercuric Chloride;
Metals;
Neprilysin;
PC12 Cells*
- From:Toxicological Research
2013;29(4):235-240
- CountryRepublic of Korea
- Language:English
-
Abstract:
Extracellular accumulation of amyloid beta protein (Abeta) plays a central role in Alzheimer's disease (AD). Some metals, such as copper, lead, and aluminum can affect the Abeta accumulation in the brain. However, the effect of mercury on Abeta accumulation in the brain is not clear. Thus, this study was proposed to estimate whether mercury concentration affects Abeta accumulation in PC12 cells. We treated 10, 100, and 1000 nM HgCl2 (Hg) or CH3HgCl2 (MeHg) for 48 hr in PC12 cells. After treatment, Abeta40 in culture medium increased in a dose- and time-dependent manner. Hg and MeHg increased amyloid precursor protein (APP), which is related to Abeta production. Neprilysin (NEP) levels in PC12 cells were decreased by Hg and MeHg treatment. These results suggested that Hg induced Abeta accumulation through APP overproduction and reduction of NEP.
