| Literature DB >> 19944163 |
Ibolya E András1, Sung Yong Eum, Wen Huang, Yu Zhong, Bernhard Hennig, Michal Toborek.
Abstract
HIV-1-infected brains are characterized by increased amyloid deposition. To study the influence of HIV-1 on amyloid beta (Abeta) homeostasis at the blood-brain barrier (BBB) level, we employed a model of brain microvascular endothelial cells exposed to HIV-1 in the presence or absence of Abeta. HIV-1 markedly increased endogenous Abeta levels and elevated accumulation of exogenous Abeta. Simvastatin, the HMG-CoA reductase inhibitor, blocked these effects. We next evaluated the effects of HIV-1 and/or simvastatin on expression of the receptor for lipoprotein related protein (LRP1) and the receptor for advanced glycation end products (RAGE), known to regulate Abeta transport across the BBB. LRP1 expression was not affected by HIV-1; however, it was increased by simvastatin. Importantly, simvastatin attenuated HIV-1-induced RAGE expression. These results suggest that HIV-1 may directly contribute to Abeta accumulation at the BBB level. In addition, statins may protect against increased Abeta levels associated with HIV-1 infection in the brain. Copyright 2009 Elsevier Inc. All rights reserved.Entities:
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Year: 2009 PMID： 19944163 PMCID： PMC2818553 DOI： 10.1016/j.mcn.2009.11.004
Source DB: PubMed Journal: Mol Cell Neurosci ISSN： 1044-7431 Impact factor: 4.314