Evidence map›Paper›PMID 33662018›Full record

ArticlePloS one2021

Polymorphic SERPINA3 prolongs oligomeric state of amyloid beta.

Maruf Mohammad Akbor, Nobuyuki Kurosawa, Hiroki Nakayama, Ayumi Nakatani, Koji Tomobe, Yoichi Chiba, Masaki Ueno, Masashi Tanaka, Yasuyuki Nomura, Masaharu Isobe

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 16 citations in OpenAlex.

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  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 1 country.

Maruf Mohammad AkborDepartment of Life Sciences and Bioengineering, Laboratory of Molecular and Cellular Biology, Faculty of Engineering, University of Toyama, Toyama, Japan.ORCID 0000-0002-5016-4535
Nobuyuki KurosawaDepartment of Life Sciences and Bioengineering, Laboratory of Molecular and Cellular Biology, Faculty of Engineering, University of Toyama, Toyama, Japan.
Hiroki NakayamaDepartment of Life Sciences and Bioengineering, Laboratory of Molecular and Cellular Biology, Faculty of Engineering, University of Toyama, Toyama, Japan.
Ayumi NakataniDepartment of Life Sciences and Bioengineering, Laboratory of Molecular and Cellular Biology, Faculty of Engineering, University of Toyama, Toyama, Japan.
Koji TomobeDepartment of Pathophysiology, Yokohama University of Pharmacy, Yokohama, Japan.
Yoichi ChibaDepartment of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Miki-cho, Kita-gun, Kagawa, Japan.
Masaki UenoDepartment of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Miki-cho, Kita-gun, Kagawa, Japan.
Masashi TanakaDepartment for Health and Longevity Research, National Institutes of Biomedical Innovation, Health and Nutrition, Shinjuku, Tokyo, Japan.
Yasuyuki NomuraDepartment of Pharmacology, School of Medicine, Kurume University, Kurume, Fukuoka, Japan.
Masaharu IsobeDepartment of Life Sciences and Bioengineering, Laboratory of Molecular and Cellular Biology, Faculty of Engineering, University of Toyama, Toyama, Japan.ORCID 0000-0003-1864-9273
University of Toyama · JPKagawa University · JPKurume University · JPNational Institute of Biomedical Innovation, Health and Nutrition · JPYokohama University of Pharmacy · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Molecular chaperon SERPINA3 colocalizes with accumulated amyloid peptide in Alzheimer's disease (AD) patient's brain. From the QTL analysis, we narrowed down Serpina3 with two SNPs in senescence-accelerated mouse prone (SAMP) 8 strain. Our study showed SAMP8 type Serpina3 prolonged retention of oligomeric Aβ 42 for longer duration (72 hr) while observing under transmission electron microscope (TEM). From Western blot results, we confirmed presence of Aβ 42 oligomeric forms (trimers, tetramers) were maintained for longer duration only in the presences of SAMP8 type Serpina3. Using SH-SY5Y neuroblastoma cell line, we observed until 36 hr preincubated Aβ 42 with SAMP8 type Serpina3 caused neuronal cell death compared to 12 hr preincubated Aβ 42 with SAMR1 or JF1 type Serpina3 proteins. Similar results were found by extending this study to analyze the effect of polymorphism of SERPINA3 gene of the Japanese SNP database for geriatric research (JG-SNP). We observed that polymorphic SERPINA3 I308T (rs142398813) prolonged toxic oligomeric Aβ 42 forms till 48 hr in comparison to the presence wild type SERPINA3 protein, resulting neuronal cell death. From this study, we first clarified pathogenic regulatory role of polymorphic SERPINA3 in neurodegeneration.

Indexed as

Polymorphism, Single NucleotideAcute-Phase ProteinsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCell Line, TumorHumansMaleMicePeptide FragmentsProtein MultimerizationQuantitative Trait LociSerpinsAcute-Phase ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-42)Peptide FragmentsSerpina3n protein, mouseSERPINA3 protein, humanSerpins

Identifiers

PMID33662018
PMCPMC7932536
OpenAlexW3135544922

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.