| http://purl.uniprot.org/citations/22745485 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22745485 | http://www.w3.org/2000/01/rdf-schema#comment | "The blood-brain barrier (BBB), which is formed by adherens and tight junctions (TJs) of endothelial cells, maintains homeostasis of the brain. Disrupted intracellular Ca²⁺ homeostasis and breakdown of the BBB have been implicated in the pathogenesis of Alzheimer's disease (AD). The receptor for advanced glycation end products (RAGE) is known to interact with amyloid β-peptide (Aβ) and mediate Aβ transport across the BBB, contributing to the deposition of Aβ in the brain. However, molecular mechanisms underlying Aβ-RAGE interaction-induced alterations in the BBB have not been identified. We found that Aβ₁₋₄₂ induces enhanced permeability, disruption of zonula occludin-1 (ZO-1) expression in the plasma membrane, and increased intracellular calcium and matrix metalloproteinase (MMP) secretion in cultured endothelial cells. Neutralizing antibodies against RAGE and inhibitors of calcineurin and MMPs prevented Aβ₁₋₄₂-induced changes in ZO-1, suggesting that Aβ-RAGE interactions alter TJ proteins through the Ca²⁺-calcineurin pathway. Consistent with these in vitro findings, we found disrupted microvessels near Aβ plaque-deposited areas, elevated RAGE expression, and enhanced MMP secretion in microvessels of the brains of 5XFAD mice, an animal model for AD. We have identified a potential molecular pathway underlying Aβ-RAGE interaction-induced breakage of BBB integrity. This pathway might play an important role in the pathogenesis of AD."xsd:string |
| http://purl.uniprot.org/citations/22745485 | http://purl.org/dc/terms/identifier | "doi:10.1523/jneurosci.6102-11.2012"xsd:string |
| http://purl.uniprot.org/citations/22745485 | http://purl.uniprot.org/core/author | "Chang S."xsd:string |
| http://purl.uniprot.org/citations/22745485 | http://purl.uniprot.org/core/author | "Hong H.S."xsd:string |
| http://purl.uniprot.org/citations/22745485 | http://purl.uniprot.org/core/author | "Moon M."xsd:string |
| http://purl.uniprot.org/citations/22745485 | http://purl.uniprot.org/core/author | "Ha C.M."xsd:string |
| http://purl.uniprot.org/citations/22745485 | http://purl.uniprot.org/core/author | "Mook-Jung I."xsd:string |
| http://purl.uniprot.org/citations/22745485 | http://purl.uniprot.org/core/author | "Kook S.Y."xsd:string |
| http://purl.uniprot.org/citations/22745485 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22745485 | http://purl.uniprot.org/core/name | "J Neurosci"xsd:string |
| http://purl.uniprot.org/citations/22745485 | http://purl.uniprot.org/core/pages | "8845-8854"xsd:string |
| http://purl.uniprot.org/citations/22745485 | http://purl.uniprot.org/core/title | "Abeta(1)₋(4)(2)-RAGE interaction disrupts tight junctions of the blood-brain barrier via Ca^2⁺-calcineurin signaling."xsd:string |
| http://purl.uniprot.org/citations/22745485 | http://purl.uniprot.org/core/volume | "32"xsd:string |
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