Evidence map›Paper›PMID 28116173›Full record

ArticleNeural plasticity2017

Electroacupuncture Regulates Hippocampal Synaptic Plasticity via miR-134-Mediated LIMK1 Function in Rats with Ischemic Stroke.

Weilin Liu, Jie Wu, Jia Huang, Peiyuan Zhuo, Yunjiao Lin, Lulu Wang, Ruhui Lin, Lidian Chen, Jing Tao

Open access · goldAbstract read
In one paragraph

Article in Neural plasticity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
4.5field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
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  14. New epigenetic players in stroke pathogenesis: From non-coding RNAs to exosomal non-coding RNAs.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
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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

9 authors at 1 institution in 1 country.

Weilin LiuCollege of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, China.
Jie WuFujian Key Laboratory of Rehabilitation Technology, Fuzhou, Fujian 350122, China.
Jia HuangCollege of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, China.ORCID 0000-0002-0976-9882
Peiyuan ZhuoFujian Key Laboratory of Rehabilitation Technology, Fuzhou, Fujian 350122, China.
Yunjiao LinFujian Key Laboratory of Rehabilitation Technology, Fuzhou, Fujian 350122, China.
Lulu WangFujian Key Laboratory of Rehabilitation Technology, Fuzhou, Fujian 350122, China.
Ruhui LinFujian Key Laboratory of Rehabilitation Technology, Fuzhou, Fujian 350122, China.
Lidian ChenCollege of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, China.ORCID 0000-0003-1944-4798
Jing TaoCollege of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, China.ORCID 0000-0001-9751-5294
Fujian University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MircoRNAs (miRs) have been implicated in learning and memory, by regulating LIM domain kinase (LIMK1) to induce synaptic-dendritic plasticity. The study aimed to investigate whether miRNAs/LIMK1 signaling was involved in electroacupuncture- (EA-) mediated synaptic-dendritic plasticity in a rat model of middle cerebral artery occlusion induced cognitive deficit (MICD). Compared to untreatment or non-acupoint-EA treatment, EA at DU20 and DU24 acupoints could shorten escape latency and increase the frequency of crossing platform in Morris water maze test. T2-weighted imaging showed that the MICD rat brain lesions were located in cortex, hippocampus, corpus striatum, and thalamus regions and injured volumes were reduced after EA. Furthermore, we found that the density of dendritic spine and the number of synapses in the hippocampal CA1 pyramidal cells were obviously reduced at Day 14 after MICD. However, synaptic-dendritic loss could be rescued after EA. Moreover, the synaptic-dendritic plasticity was associated with increases of the total LIMK1 and phospho-LIMK1 levels in hippocampal CA1 region, wherein EA decreased the expression of miR-134, negatively regulating LIMK1 to enhance synaptic-dendritic plasticity. Therefore, miR-134-mediated LIMK1 was involved in EA-induced hippocampal synaptic plasticity, which served as a contributor to improving learning and memory during the recovery stage of ischemic stroke.

Indexed as

ElectroacupunctureNeuronal PlasticityAnimalsBrainBrain IschemiaCA1 Region, HippocampalCognitive DysfunctionDendritic SpinesLim KinasesMaleMaze LearningMicroRNAsPyramidal CellsRatsRats, Sprague-DawleyStrokeLimk1 protein, ratLim KinasesMicroRNAsMIRN134 microRNA, rat

Identifiers

PMID28116173
PMCPMC5237739
OpenAlexW2565133415

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Read underepoch 390

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.