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KMID : 1034820130090010057
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Molecular & Cellular Toxicology
2013 Volume.9 No. 1 p.57 ~ p.66
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Copper induces the accumulation of amyloid-beta in the brain
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Kim Dong-Kyeong
Song Ji-Won
Park Jung-Duck
Choi Byung-Sun
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Abstract
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Cu(II) increased the levels of Aβ(40) and Aβ(42) in the PC12 cell medium in a dose-dependent manner compared with control. The mRNA and protein expression levels of APP and BACE1, which play an important role in Aβ generation, were increased in the PC12 cells exposed to Cu(II). NEP expression levels in mRNA and protein were decreased in a dose-dependent manner in PC12 cells treated with Cu(II). In the RBE4 cells, Cu(II) decreased LRP1 levels and increased RAGE levels in mRNA and protein compared with control. Moreover, Cu(II) decreased the clearance of Aβ using the blood-brain barrier (BBB) transport study. However, in the Z310 cells, Cu(II) didn’t change the levels of LRP1 and RAGE in mRNA and protein. These results implied that Cu(II) increased Aβ accumulation in the brain by increasing Aβ production but decreasing Aβ degradation in the brain parenchyma and interfering with clearance of Aβ via the BBB.
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KEYWORD
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Amyloid beta protein, Amyloid precursor protein (APP), Beta-site APP-cleaving enzyme 1 (BACE1), Blood-brain barrier (BBB), Blood-CSF barrier (BCB), Copper, Neprilysin (NEP), Low-density lipoprotein receptor related protein 1 (LRP1), Receptor for advanced glycation end products (RAGE)
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