Cited by 90

LRP promotes endocytosis and degradation, but not transcytosis, of the amyloid-β peptide in a blood–brain barrier in vitro model

Nazer, Babak, Hong, Soyon, Selkoe, Dennis J.·2008·Neurobiology of Disease

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Crossref · 10.1016/j.nbd.2007.12.005

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  • Conflicting findings on LRP1 in previous studies might be due to Aβ injections at concentrations beyond physiological relevance into different brain regions or the use of epithelial cells such as MDCK and CHO cells for in vitro studies.

    “These results might be due to Aβ injections at concentrations beyond physiological relevance into different brain regions (17, 18, 52) or the use of epithelial cells, such as MDCK and CHO cells (5,19), for in vitro studies.”

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Research works printed but not linked: 23

  1. Bakos, 1998, Functional multidrug resistance protein (MRP1) lacking the N-terminal transmembrane domain, J. Biol. Chem., 273, 32167, 10.1074/jbc.273.48.32167 · DOI
  2. Brandli, 1990, Transcytosis in MDCK cells: identification of glycoproteins transported bidirectionally between both plasma membrane domains, J. Cell Biol., 111, 2909, 10.1083/jcb.111.6.2909 · DOI
  3. Cam, 2006, Modulation of beta-amyloid precursor protein trafficking and processing by the low density lipoprotein receptor family, Mol. Neurodegener., 1, 8, 10.1186/1750-1326-1-8 · DOI · Paper page
  4. Deane, 2004, LRP/amyloid beta-peptide interaction mediates differential brain efflux of Abeta isoforms, Neuron, 43, 333, 10.1016/j.neuron.2004.07.017 · DOI · Paper page
  5. Garberg, 2005, In vitro models for the blood–brain barrier, Toxicol. In Vitro, 19, 299, 10.1016/j.tiv.2004.06.011 · DOI
  6. Gumbleton, 2001, Progress and limitations in the use of in vitro cell cultures to serve as a permeability screen for the blood–brain barrier, J. Pharm. Sci., 90, 1681, 10.1002/jps.1119 · DOI
  7. Haass, 1994, Polarized secretion of beta-amyloid precursor protein and amyloid beta-peptide in MDCK cells, Proc. Natl. Acad. Sci. U. S. A., 91, 1564, 10.1073/pnas.91.4.1564 · DOI
  8. Hardy, 2002, The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics, Science, 297, 353, 10.1126/science.1072994 · DOI · Paper page
  9. Hunziker, 1989, Expression of macrophage-lymphocyte Fc receptors in Madin–Darby canine kidney cells: polarity and transcytosis differ for isoforms with or without coated pit localization domains, J. Cell Biol., 109, 3291, 10.1083/jcb.109.6.3291 · DOI
  10. Irvine, 1999, MDCK (Madin–Darby canine kidney) cells: a tool for membrane permeability screening, J. Pharm. Sci., 88, 28, 10.1021/js9803205 · DOI
  11. Kang, 1997, Genetic association of the low-density lipoprotein receptor-related protein gene (LRP), an apolipoprotein E receptor, with late-onset Alzheimer’s disease, Neurology, 49, 56, 10.1212/WNL.49.1.56 · DOI · Paper page
  12. Krieger, 1994, Structures and functions of multiligand lipoprotein receptors: macrophage scavenger receptors and LDL receptor-related protein (LRP), Annu. Rev. Biochem., 63, 601, 10.1146/annurev.bi.63.070194.003125 · DOI
  13. Lalloo, 2004, Membrane transport of camptothecin: facilitation by human P-glycoprotein (ABCB1) and multidrug resistance protein 2 (ABCC2), BMC Med., 2, 16, 10.1186/1741-7015-2-16 · DOI
  14. Marzolo, 2003, Differential distribution of low-density lipoprotein-receptor-related protein (LRP) and megalin in polarized epithelial cells is determined by their cytoplasmic domains, Traffic, 4, 273, 10.1034/j.1600-0854.2003.00081.x · DOI · Paper page
  15. Obermoeller-McCormick, 2001, Dissection of receptor folding and ligand-binding property with functional minireceptors of LDL receptor-related protein, J. Cell Sci., 114, 899, 10.1242/jcs.114.5.899 · DOI · Paper page
  16. Rubin, 1999, The cell biology of the blood–brain barrier, Annu. Rev. Neurosci., 22, 11, 10.1146/annurev.neuro.22.1.11 · DOI
  17. Selkoe, 2003, Alzheimer’s disease: molecular understanding predicts amyloid-based therapeutics, Annu. Rev. Pharmacol. Toxicol., 43, 545, 10.1146/annurev.pharmtox.43.100901.140248 · DOI
  18. Sharom, 1997, The P-glycoprotein efflux pump: how does it transport drugs?, J. Membr. Biol., 160, 161, 10.1007/s002329900305 · DOI
  19. Silverberg, 2003, Alzheimer’s disease, normal-pressure hydrocephalus, and senescent changes in CSF circulatory physiology: a hypothesis, Lancet Neurol., 2, 506, 10.1016/S1474-4422(03)00487-3 · DOI
  20. Tanzi, 2004, Clearance of Alzheimer’s Abeta peptide: the many roads to perdition, Neuron, 43, 605, 10.1016/S0896-6273(04)00533-1 · DOI
  21. Weiner, 2006, Immunology and immunotherapy of Alzheimer’s disease, Nat. Rev. Immunol., 6, 404, 10.1038/nri1843 · DOI · Paper page
  22. Weksler, 2005, Blood–brain barrier-specific properties of a human adult brain endothelial cell line, Faseb J., 19, 1872, 10.1096/fj.04-3458fje · DOI
  23. Zlokovic, 2004, Clearing amyloid through the blood–brain barrier, J. Neurochem., 89, 807, 10.1111/j.1471-4159.2004.02385.x · DOI · Paper page

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Metadata

Authors
Nazer, B., Hong, S., & Selkoe, D. J.
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2008-04
Volume
30
Issue
1
Pages
94-102
ISSN
0969-9961
Cited by
90
References
4
Language
en

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