Evidence map›Paper›PMID 30975733›Full record

ArticleBioscience reports2019

MicroRNA-153 promotes brain-derived neurotrophic factor and hippocampal neuron proliferation to alleviate autism symptoms through inhibition of JAK-STAT pathway by LEPR.

Yu-Hui You, Zhi-Qiang Qin, Huan-Li Zhang, Zhao-Hong Yuan, Xin Yu

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Cognitive and Motor Dysfunction in STXBP1 R406H Mice.Journal of molecular neuroscience : MN · 2026
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  19. Recent Progress on Relevant microRNAs in Autism Spectrum Disorders.International journal of molecular sciences · 2020
    Review
  20. 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

5 authors at 1 institution in 1 country.

Yu-Hui YouDepartment of Paediatric Rehabilitation, Affiliated Hospital of Jining Medical University, Jining 272029, P.R. China.
Zhi-Qiang QinDepartment of Paediatric Rehabilitation, Affiliated Hospital of Jining Medical University, Jining 272029, P.R. China.
Huan-Li ZhangDepartment of Paediatric Rehabilitation, Affiliated Hospital of Jining Medical University, Jining 272029, P.R. China.
Zhao-Hong YuanDepartment of Paediatric Rehabilitation, Affiliated Hospital of Jining Medical University, Jining 272029, P.R. China.
Xin YuDepartment of Paediatric Rehabilitation, Affiliated Hospital of Jining Medical University, Jining 272029, P.R. China yuxin_jn@163.com.ORCID 0000-0002-1972-5576
Affiliated Hospital of Jining Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism is known as a severe neurobehavioral syndrome, with males affected more often than females. Previous studies have revealed that microRNAs (miRNAs) play a critical role in the search for novel therapeutic strategies for autism. Therefore, we evaluate the ability of miR-153 to influence brain-derived neurotrophic factor (BDNF) of autism as well as proliferation and apoptosis of hippocampal neuron through the janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway by targeting leptin receptor (LEPR). Firstly, the autistic mice models were established and Morris water maze was employed for the analysis of the learning ability and memory of the mice. Besides, in vitro experiments were conducted with the transfection of different mimic, inhibitor, or siRNA into the hippocampal neuron cells, after which the effect of miR-153 on LEPR and the JAK-STAT signaling pathway-related factors was investigated. Next, 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide assay and flow cytometry assay were conducted to evaluate cell proliferation, cell cycle, and apoptosis respectively following transfection. The results revealed that there was a significant decrease in learning ability and memory in the autistic mice along with a reduction in the positive expression rate of BDNF and serious inflammatory reaction. LEPR was confirmed as a target gene of miR-153 by the dual luciferase reporter gene assay. After transfection of overexpressed miR-153, LEPR and the JAK-STAT signaling pathway were inhibited followed by an increase in BDNF and enhancement of cell proliferation. In conclusion, the high expression of miR-153 can inhibit activation of JAK-STAT signaling pathway by LEPR, thus improving BDNF expression and the proliferative ability of hippocampal neurons.

Indexed as

AnimalsApoptosisAutistic DisorderBrain-Derived Neurotrophic FactorCell CycleCell ProliferationDisease Models, AnimalFemaleGene Expression RegulationHippocampusHumansJanus KinasesMiceMicroRNAsNeuronsReceptors, LeptinBdnf protein, mouseBrain-Derived Neurotrophic FactorJanus Kinasesleptin receptor, mouseMicroRNAsMIRN153 microRNA, mouseReceptors, LeptinRNA, Small InterferingSTAT Transcription FactorsAutismBrain-derived neurotrophic factorHippocampal neuronsJAK-STAT signaling pathwaymicroRNA-153Proliferation

Identifiers

PMID30975733
PMCPMC6591574
OpenAlexW2939222410

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.