Abstract
MicroRNA alterations and axonopathy have been reported in patients with Alzheimer's disease (AD) and in AD mouse models. We now report that miR-342-5p is upregulated in APP/PS1, PS1ΔE9, and PS1-M146V transgenic AD mice, and that this upregulation is mechanistically linked to elevated β-catenin, c-Myc, and interferon regulatory factor-9. The increased miR-342-5p downregulates the expression of ankyrin G (AnkG), a protein that is known to play a critical role at the axon initial segment. Thus, a specific miRNA alteration may contribute to AD axonopathy by downregulating AnkG.
Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alzheimer Disease / genetics
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Alzheimer Disease / metabolism*
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Amyloid beta-Protein Precursor / genetics
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Animals
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Ankyrins / genetics
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Ankyrins / metabolism*
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Axons / metabolism
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Cells, Cultured
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Humans
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Interferon-Stimulated Gene Factor 3, gamma Subunit / genetics
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Interferon-Stimulated Gene Factor 3, gamma Subunit / metabolism
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Mice
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MicroRNAs / genetics
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MicroRNAs / metabolism*
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Presenilin-1 / genetics
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Proto-Oncogene Proteins c-myc / genetics
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Proto-Oncogene Proteins c-myc / metabolism
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beta Catenin / genetics
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beta Catenin / metabolism
Substances
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Amyloid beta-Protein Precursor
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Ank3 protein, mouse
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Ankyrins
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Interferon-Stimulated Gene Factor 3, gamma Subunit
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MicroRNAs
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Mirn342 microRNA, mouse
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Presenilin-1
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Proto-Oncogene Proteins c-myc
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beta Catenin