期刊
NEUROCHEMICAL RESEARCH
卷 36, 期 1, 页码 49-57出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-010-0260-x
关键词
Insulin-like growth factor 1; beta-Site amyloid precursor protein cleaving enzyme 1; beta-Amyloid peptides; PI3-K/Akt signaling pathway; MAPK/ERK1/2 signaling pathway
资金
- Chongqing Key Laboratory of Neurology, Chongqing Medical University
Insulin-like growth factor 1 (IGF-1) stimulates a-secretase processing of amyloid precursor protein (APP) and decreases A beta production. Little is known about the relationship between IGF-1 and beta-site amyloid precursor protein cleaving enzyme 1 (BACE-1), the protease essential for the production of beta-amyloid peptides (A beta). Here, we investigated the effect of IGF-1 on BACE-1 in PC12 cells. Quantitative polymerase chain reaction analysis and western blot showed that treatment of cells with IGF-1 significantly decreased the levels of BACE-1 mRNA and protein. Furthermore, IGF-1 increased the phosphorylation of Akt and ERK1/2. The presence of the phosphatidylinositol 3-kinase (PI3-K) inhibitor LY294002 and the mitogen-activated protein kinase kinases (MEK) inhibitor PD98059 blocked the effect of IGF-1 on BACE-1. Our data indicated that IGF-1-induced reduction of BACE-1 might involve the PI3-K/Akt and MAPK/ERK1/2 signaling pathways.
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