Evidence map›Paper›PMID 29808547›Full record

ArticleCNS neuroscience & therapeutics2019

MiR-181b inhibits P38/JNK signaling pathway to attenuate autophagy and apoptosis in juvenile rats with kainic acid-induced epilepsy via targeting TLR4.

Li Wang, Li-Fang Song, Xiao-Yi Chen, Yan-Li Ma, Jun-Fang Suo, Jing-He Shi, Guo-Hong Chen

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

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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 1 institution in 1 country.

Li WangDepartment of Neurology, Zhengzhou Children's Hospital (Zhengzhou University Affiliated Children's Hospital), Zhengzhou, China.
Li-Fang SongDepartment of Neurology, Zhengzhou Children's Hospital (Zhengzhou University Affiliated Children's Hospital), Zhengzhou, China.
Xiao-Yi ChenDepartment of Neurology, Zhengzhou Children's Hospital (Zhengzhou University Affiliated Children's Hospital), Zhengzhou, China.
Yan-Li MaDepartment of Neurology, Zhengzhou Children's Hospital (Zhengzhou University Affiliated Children's Hospital), Zhengzhou, China.
Jun-Fang SuoDepartment of Neurology, Zhengzhou Children's Hospital (Zhengzhou University Affiliated Children's Hospital), Zhengzhou, China.
Jing-He ShiDepartment of Neurology, Zhengzhou Children's Hospital (Zhengzhou University Affiliated Children's Hospital), Zhengzhou, China.
Guo-Hong ChenDepartment of Neurology, Zhengzhou Children's Hospital (Zhengzhou University Affiliated Children's Hospital), Zhengzhou, China.ORCID 0000-0003-2489-3600
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo explore the role of miR-181b in alterations of apoptosis and autophagy in the kainic acid (KA)-induced epileptic juvenile rats via modulating TLR4 and P38/JNK signaling pathway.

methodsDual-luciferase reporter assay was performed to testify the targeting relationship between miR-181b and TLR4. After intracerebroventricular injection (i.c.v.) of KA, rats were injected with miR-181b agomir and TLR4 inhibitor (TAK-242). The TLR-4 activator lipopolysaccharide (LPS) was also administered into rats immediately after injection with miR-181b agomir. Quantitative real-time-polymerase chain reaction (qRT-PCR) was used for detections of miR-181b and TLR4 expressions, hematoxylin-eosin (HE) and Nissl staining for observation of the hippocampus morphological changes, and TUNEL staining for apoptosis analysis. Moreover, western blot was determined to detect TLR4 and P38/JNK pathway proteins, as well as autophagy- and apoptosis-related proteins.

resultsTLR4 was identified as a direct target of miR-181b using Dual-luciferase reporter assay. KA rats injected with miR-181b agomir or TAK-242 had improved learning and memory abilities, reduced seizure severity of Racine's scale, and lessened neuron injury. Additionally, miR-181b agomir or TAK-242 could significantly inhibit P38/JNK signaling, decrease LC3II/I, Beclin-1, ATG5, ATG7, ATG12, Bax, and cleaved caspases-3, but increase p62 and Bcl-2 expression. No significances were found between KA group and KA + miR-181b + LPS group.

conclusionMiR-181b could inhibit P38/JNK signaling pathway via targeting TLR4, thereby exerting protective roles in attenuating autophagy and apoptosis of KA-induced epileptic juvenile rats.

Indexed as

AnimalsApoptosisAutophagyDisease Models, AnimalEpilepsyFemaleHippocampusKainic AcidMaleMAP Kinase Kinase 4MAP Kinase Signaling SystemMicroRNAsNeuroprotectionp38 Mitogen-Activated Protein KinasesRandom AllocationRats, WistarKainic AcidMAP Kinase Kinase 4MicroRNAsMIRN181 microRNA, ratp38 Mitogen-Activated Protein KinasesTlr4 protein, ratToll-Like Receptor 4apoptosisautophagyepilepsymiR-181bP38/JNKTLR4

Identifiers

PMID29808547
PMCPMC6436603
OpenAlexW2807632155

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.