Cited by 127Alzheimer's disease research and treatmentsLysosomal Storage Disorders ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Reactivity of Apolipoprotein E4 and Amyloid β Peptide

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Ji, Zhong-Sheng, Müllendorff, Karin, Cheng, Irene H., Miranda, R. Dennis, Huang, Yadong, Mahley, Robert W.·2006·Journal of Biological Chemistry

DOI 10.1074/jbc.m506646200

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Abstract

We previously demonstrated that apolipoprotein E4 (apoE4) potentiates lysosomal leakage and apoptosis induced by amyloid beta (Abeta) peptide in cultured Neuro-2a cells and hypothesized that the low pH of lysosomes accentuates the conversion of apoE4 to a molten globule, inducing reactive intermediates capable of destabilizing cellular membranes. Here we report that neutralizing lysosomal pH with bafilomycin or NH4Cl abolished the apoE4 potentiation of Abeta-induced lysosomal leakage and apoptosis in Neuro-2a cells. Consistent with these results, apoE4 at acidic pH bound more avidly to phospholipid vesicles and disrupted them to a greater extent than at pH 7.4. Comparison of "Arctic" mutant Abeta, which forms multimers, and GM6 mutant Abeta, which remains primarily monomeric, showed that aggregation is essential for apoE4 to potentiate Abeta-induced lysosomal leakage and apoptosis. Both apoE4 and Abeta1-42 had to be internalized to exert these effects. Blocking the low density lipoprotein receptor-related protein with small interfering RNA abolished the enhanced effects of apoE4 and Abeta on lysosomes and apoptosis. In cultured Neuro-2a cells, Abeta1-42 increased lysosome formation to a greater extent in apoE3- or apoE4-transfected cells than in Neo-transfected cells, as shown by immunostaining for lysosome-associated membrane protein 1. Similarly, in transgenic mice expressing apoE and amyloid precursor protein, hippocampal neurons displayed increased numbers of lysosomes. Thus, apoE4 and Abeta1-42 may work in concert in neurons to increase lysosome formation while increasing the susceptibility of lysosomal membranes to disruption, release of lysosomal enzymes into the cytosol, and neuronal degeneration.

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Authors: Ji, Z.-S., Müllendorff, K., Cheng, I. H., Miranda, R. D., Huang, Y., & Mahley, R. W.
Affiliations: University of California, San Francisco (US)
Corresponding author: Mahley, Robert W.
ORCID: Cheng, Irene H.
Huang, Yadong
Mahley, Robert W.
Venue: Journal of Biological Chemistry
Publisher: Elsevier BV
Published: 2006-02
Volume: 281
Issue: 5
Pages: 2683-2692
ISSN: 0021-9258 (ISSN-L)
DOI: 10.1074/jbc.m506646200
OpenAlex: W2048371394
Cited by: 127
References: 78
Citations by year: 2026: 2 · 2025: 3 · 2024: 5 · 2023: 1 · 2022: 7 · 2021: 6 · 2020: 12 · 2019: 9 · 2018: 6 · 2017: 7 · 2016: 9 · 2015: 3 · 2014: 2 · 2013: 5 · 2012: 6
FWCI: 4.59
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
creativecommons.org/licenses/by/4.0/ (vor, 5359 d)
Locations: Journal of Biological Chemistry (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: National Institutes of Health (1c06rr018928-01)
National Institute on Aging (P01AG022074)
National Institute of Neurological Disorders and Stroke (R21NS046465)
National Center for Research Resources (C06RR18928)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Genetics (clinical) › Lysosomal Storage Disorders Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: APOE ε4, amyloid-beta, apoptosis, lysosomal pH, molten globule, lysosomal membrane disruption, amyloid fibril formation, amyloid-beta 42, low density lipoprotein receptor-related protein, lysosome-associated membrane protein 1, lysosome formation, hippocampal neurons, Alzheimer's disease, N2a cells
MeSH terms: Animals, Apolipoproteins E, Cell Line, Humans, Hydrogen-Ion Concentration, Intracellular Membranes, Liposomes, Lysosomes, Mice, Transgenic, Neurons, Transfection, Amyloid beta-Peptides, Apoptosis, Dimerization, Neurodegenerative Diseases, Mice, Apolipoprotein E4

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Reactivity of Apolipoprotein E4 and Amyloid β Peptide

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