Evidence map›Paper›PMID 29464486›Full record

ArticleNeurochemical research2018

MicroRNA-322 Cluster Promotes Tau Phosphorylation via Targeting Brain-Derived Neurotrophic Factor.

Jun Zhang, Zanchao Liu, Yuanyuan Pei, Wen Yang, Chicu Xie, Shiqi Long

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

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  17. Non-coding RNA influences in dementia.Non-coding RNA research · 2018
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Jun ZhangDepartment of Pathology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, People's Republic of China.
Zanchao LiuThe Shijiazhuang Second Hospital of Hebei Province, Shijiazhuang, 050051, People's Republic of China.
Yuanyuan PeiDepartment of Pathology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, People's Republic of China.
Wen YangDepartment of Pathology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, People's Republic of China.
Chicu XieDepartment of Immunology, Basic School of Medicine, Guizhou Medical University, Guiyang, 550004, People's Republic of China.
Shiqi LongDepartment of Immunology, Basic School of Medicine, Guizhou Medical University, Guiyang, 550004, People's Republic of China. 767446430@qq.com.
Guiyang Medical University · CNAffiliated Hospital of Guizhou Medical University · CNHospital of Hebei Province · CN

Funding

Science and Technology foundation of Guizhou Province TN2015-60Science and Technology Foundation of Guizhou Province (CN) J-2014-2017the National Health and Family Planning Commission of Guizhou Province WT2017-14
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) is a crucial regulator to support synaptic plasticity and neuronal survival, its significant decrease is a pathophysiological hallmark in Alzheimer's disease (AD) brains and accounts for poor prognosis. MicroRNAs (miRNAs) interfere with the translation of target mRNAs and control a variety of physiological and pathological processes. MiR-322 is the rodent homologue of human miR-424, it is involved in the modulation of cell differentiation, proliferation, apoptosis and metabolic activities in diverse tissues and organs. However, the roles and potential mechanisms of miR-322 remain elusive in AD pathogenesis. Here we observed miR-322 is significantly increased along with BDNF decrease in AD mouse brain. Bioinformatics prediction implicated that BDNF 3'-untranslated region (3'-UTR) possesses the putative target sequence of miR-322. Luciferase reporter assay identified that miR-322 can directly conjugate to BDNF 3'-UTR. The functional research showed that MiR-322 input deregulates BDNF expression at either mRNA or protein levels, whereas miR-322 silence restores BDNF expression in vitro. Furthermore, we found miR-322 promotes Tau phosphorylation via negatively controlling BDNF-TrkB receptor activation, otherwise MiR-322 silence restores TrkB activation and attenuates tau phosphorylation. Collectively, this study demonstrated a novel miRNA-dependent manner of BDNF degradation in AD pathogenesis, it may drive a miRNAs- or BDNF based therapeutic strategies against Alzheimer's disease.

Indexed as

Alzheimer DiseaseAnimalsBrainBrain-Derived Neurotrophic FactorHumansMiceMicroRNAsNeuronal PlasticityNeuronsPhosphorylationtau ProteinsBrain-Derived Neurotrophic FactorMAPT protein, humanMapt protein, mouseMicroRNAsMIRN322 microRNA, mouseMIRN424 microrna, humantau ProteinsAlzheimer’s diseaseBDNF–TrkB signalMicroRNA-322Tau phosphorylation

Identifiers

PMID29464486
OpenAlexW2789344207

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.