Engulfment of Toxic Amyloid β-protein in Neurons and Astrocytes Mediated by MEGF10.


Journal

Neuroscience
ISSN: 1873-7544
Titre abrégé: Neuroscience
Pays: United States
ID NLM: 7605074

Informations de publication

Date de publication:
01 09 2020
Historique:
received: 19 03 2020
revised: 30 06 2020
accepted: 10 07 2020
pubmed: 20 7 2020
medline: 15 5 2021
entrez: 20 7 2020
Statut: ppublish

Résumé

Amyloid-β proteins (A β), including Aβ42 and A β 43, are known pathogenesis factors of Alzheimer's disease (AD). Unwanted substances in the brain, including A β, are generally removed by microglia, astrocytes, or neurons via a phagocytosis receptor. We observed that neurons and astrocytes engulfed A β 42 and A β 43, which are more neurotoxic than A β 40. We previously showed that multiple-EGF like domains 10 (MEGF10) plays an important role in apoptotic cell elimination and is expressed in mammalian neurons and astrocytes. Therefore, we assessed whether MEGF10 is involved in A β42 and A β43 engulfment in MEGF10-expressing neurons and astrocytes. We found that MEGF10-expressing astrocytes and neurons engulfed A β42 and A β43 but not A β40. Furthermore, incubation of the neurons and astrocytes with A β42 and A β43a ugmented MEGF10 phosphorylation; however, incubation with A β40 did not have this augmenting effect. Our findings suggest that MEGF10 plays a phagocytosis receptor function for A β42 and A β43 in neurons and astrocytes.

Identifiants

pubmed: 32682823
pii: S0306-4522(20)30449-8
doi: 10.1016/j.neuroscience.2020.07.016
pii:
doi:

Substances chimiques

Amyloid beta-Peptides 0
Membrane Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1-7

Informations de copyright

Copyright © 2020 IBRO. Published by Elsevier Ltd. All rights reserved.

Auteurs

Yu Fujita (Y)

Department of Neuroscience, School of Pharmacy, Iwate Medical University, 2-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan. Electronic address: yufujita@iwate-med.ac.jp.

Tomoji Maeda (T)

Department of Pharmacology, Nihon Pharmaceutical University, 10281 Komuro, Ina-machi, Kitaadachi-gun, Saitama 362-0806, Japan.

Chiharu Sato (C)

Department of Neuroscience, School of Pharmacy, Iwate Medical University, 2-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan.

Masaya Sato (M)

Department of Neuroscience, School of Pharmacy, Iwate Medical University, 2-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan.

Hatsune Hatakeyama (H)

Department of Neuroscience, School of Pharmacy, Iwate Medical University, 2-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan.

Yume Ota (Y)

Department of Neuroscience, School of Pharmacy, Iwate Medical University, 2-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan.

Nozomi Iwabuchi (N)

Department of Neuroscience, School of Pharmacy, Iwate Medical University, 2-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan.

Komaki Tatesawa (K)

Department of Neuroscience, School of Pharmacy, Iwate Medical University, 2-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan.

Ayako Nomura (A)

Department of Neuroscience, School of Pharmacy, Iwate Medical University, 2-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan.

Kun Zou (K)

Department of Biochemistry, School of Medicine, Nagoya City University, Nagoya, Japan.

Hiroto Komano (H)

Department of Neuroscience, School of Pharmacy, Iwate Medical University, 2-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan. Electronic address: hkomano@iwate-med.ac.jp.

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Classifications MeSH