Toxic effects of endoplasmic reticulum stress transducer BBF2H7-derived small peptide fragments on neuronal cells.


Journal

Brain research
ISSN: 1872-6240
Titre abrégé: Brain Res
Pays: Netherlands
ID NLM: 0045503

Informations de publication

Date de publication:
15 12 2020
Historique:
received: 08 06 2020
revised: 10 09 2020
accepted: 26 09 2020
pubmed: 4 10 2020
medline: 28 10 2021
entrez: 3 10 2020
Statut: ppublish

Résumé

Aggregation, fibril formation, and deposition of amyloid β (Aβ) protein are believed to be the central pathogeneses of Alzheimer's disease (AD). Numerous studies have shown that fibril formation is promoted by preformed seeds at the beginning of the aggregation process. Therefore, aggregated molecules that promote fibrillization of Aβ protein as seeds could affect the pathology. We recently found that approximately 40 amino acid hydrophobic peptides, BBF2H7-derived small peptide (BSP) fragments, are generated via intramembranous cleavage under endoplasmic reticulum (ER) stress conditions. Interestingly, similar to Aβ protein, the fragments exhibit a high aggregation propensity and form fibril structures. It has been noted that ER stress is involved in the pathogenesis of AD. In this study, we examined the effect of BSP fragments on aggregation and cytotoxicity of Aβ

Identifiants

pubmed: 33010207
pii: S0006-8993(20)30497-2
doi: 10.1016/j.brainres.2020.147139
pii:
doi:

Substances chimiques

Amyloid 0
Amyloid beta-Peptides 0
Basic-Leucine Zipper Transcription Factors 0
CREB3L2 protein, human 0
Peptide Fragments 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

147139

Informations de copyright

Copyright © 2020 The Author(s). Published by Elsevier B.V. All rights reserved.

Auteurs

Koji Matsuhisa (K)

Department of Biochemistry, Institute of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan; Department of Stress Protein Processing, Institute of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.

Longjie Cai (L)

Department of Biochemistry, Institute of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.

Atsushi Saito (A)

Department of Biochemistry, Institute of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan; Department of Stress Protein Processing, Institute of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.

Fumika Sakaue (F)

Department of Stress Protein Processing, Institute of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.

Yasunao Kamikawa (Y)

Department of Stress Protein Processing, Institute of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.

Sachiko Fujiwara (S)

Department of Stress Protein Processing, Institute of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.

Rie Asada (R)

Department of Medicine, Division of Endocrinology, Metabolism, and Lipid Research, Washington University School of Medicine, St. Louis, MO 63110, USA.

Yukitsuka Kudo (Y)

Department of Gerontology and Geriatrics, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Miyagi 980-8575, Japan.

Kazunori Imaizumi (K)

Department of Biochemistry, Institute of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan. Electronic address: imaizumi@hiroshima-u.ac.jp.

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Classifications MeSH