IGF-1 Reduces BACE-1 Expression in PC12 Cells via Activation of PI3-K/Akt and MAPK/ERK1/2 Signaling Pathways |
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Authors: | Hua Zhang Ying Gao Zhengwei Dai Tao Meng Shengfen Tu Yong Yan |
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Institution: | (1) Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Chongqing, 400016, China;(2) Special Wards, The Affiliated Children Hospital of Chongqing Medical University, Chongqing, 400014, China;(3) Department of Anesthesiology, The Affiliated Children Hospital of Chongqing Medical University, Chongqing, 400014, China; |
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Abstract: | Insulin-like growth factor 1 (IGF-1) stimulates α-secretase processing of amyloid precursor protein (APP) and decreases Aβ
production. Little is known about the relationship between IGF-1 and β-site amyloid precursor protein cleaving enzyme 1 (BACE-1),
the protease essential for the production of β-amyloid peptides (Aβ). 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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