Evidence map›Paper›PMID 32307887›Full record

ArticleBrain and behavior2020

Mechanism of microRNA-22 in regulating neuroinflammation in Alzheimer's disease.

Chenyang Han, Li Guo, Yi Yang, Qiaobing Guan, Heping Shen, Yongjia Sheng, Qingcai Jiao

Open access · goldAbstract read
In one paragraph

Article in Brain and behavior, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.

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  13. New Insights on NLRP3 Inflammasome: Mechanisms of Activation, Inhibition, and Epigenetic Regulation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
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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

7 authors at 2 institutions in 1 country.

Chenyang HanState Key Laboratory of Pharmaceutical Biotechnology, School of Life Science, Nanjing University, Nanjing, China.ORCID https://orcid.org/0000-0002-2805-580X
Li GuoDepartment of Center Laboratory, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
Yi YangDepartment of Neurology, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.ORCID https://orcid.org/0000-0002-6483-7286
Qiaobing GuanDepartment of Neurology, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
Heping ShenDepartment of Neurology, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
Yongjia ShengDepartment of Pharmacy, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
Qingcai JiaoState Key Laboratory of Pharmaceutical Biotechnology, School of Life Science, Nanjing University, Nanjing, China.
Jiaxing University · CNNanjing University · CN

Funding

Natural Science Foundation of Zhejiang Province LYY19H280003
6 · The paper itself

Abstract

backgroundStudy on the expression of miRNA-22 in serum of Alzheimer's disease (AD) patients and the mechanism of neuroinflammation regulation.

methodsELISA assay was used to detect the serum level of inflammatory factors, including interleukin-1β (IL-1β), interleukin-18 (IL-18), and tumor necrosis factor-α in AD patients. TargetScan database and luciferase reporter gene assay indicated that gasdermin D (GSDMD) was the target gene of miRNA-22. miRNA-22 mimic was transfected into microglia, followed by administration of LPS and Nigericin to induce pyroptosis.

resultsIn this study, we found that the expression level of miRNA-22 in peripheral blood was lower in AD patients than that in healthy population. The expression of inflammatory factors was higher in AD patients than that in healthy people, which was negatively correlated with miRNA-22. miRNA-22 mimic could significantly inhibit pyroptosis, the expression of GSDMD and p30-GSDMD was down-regulated, the release of inflammatory factor was decreased, and the expression of NLRP3 inflammasome was down-regulated as feedback. In the APP/PS1 double transgenic mouse model, the injection of miRNA-22 mimic significantly improved the memory ability and behavior of mice. In addition, the expression of the vital protein of pyroptosis in mouse brain tissue, including GSDMD and p30-GSDMD, was down-regulated, and the expression of inflammatory factors was also decreased.

conclusionmiRNA-22 was negatively correlated with the expression of inflammatory factors in AD patients, and miRNA-22 could inhibit the release of inflammatory cytokines by regulating the inflammatory pyroptosis of glial cells via targeting GSDMD, thereby improving cognitive ability in AD mice. miRNA-22 and pyroptosis are potential novel therapeutic targets in the treatment of AD.

Indexed as

Alzheimer DiseaseMicroRNAsAnimalsHumansIntracellular Signaling Peptides and ProteinsMicePhosphate-Binding ProteinsPyroptosisIntracellular Signaling Peptides and ProteinsMicroRNAsMIRN22 microRNA, humanMirn22 microRNA, mousePhosphate-Binding ProteinsAlzheimer's diseaseinflammatory factormicrogliamicroRNA-22pyroptosis

Identifiers

PMID32307887
PMCPMC7303389
OpenAlexW3017144917

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LicenceCC BY
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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.