Evidence map›Paper›PMID 28025572›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2016

Influence of miR-155 on Cell Apoptosis in Rats with Ischemic Stroke: Role of the Ras Homolog Enriched in Brain (Rheb)/mTOR Pathway.

Guoping Xing, Zengxiang Luo, Chi Zhong, Xudong Pan, Xiaowei Xu

Abstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  3. Advancing Ischemic Stroke Prognosis: Key Role of MiR-155 Non-Coding RNA.International journal of molecular sciences · 2025
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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

5 authors at 4 institutions in 1 country.

Guoping XingDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
Zengxiang LuoDepartment of Dermatology, Affiliated Hospital of Weifang Medical University, Weifang, Shandong, China (mainland).
Chi ZhongDepartment of Neurology, Weifang People's Hospital, Weifang, Shandong, China (mainland).
Xudong PanDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
Xiaowei XuDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
Affiliated Hospital of Qingdao University · CNQingdao University · CNWeifang Medical University · CNWeifang People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND We designed and carried out this study to examine the role of miR-155 and the Rheb/mTOR pathway in ischemic stroke. We also investigated how these two elements interact with each other and contribute to injuries resulting from ischemic stroke. MATERIAL AND METHODS We used both a middle cerebral artery occlusion rat model in vivo and an oxygen-glucose deprivation cell model in vitro to simulate the onset of ischemic stroke. miR-155 mimics, miR-155 inhibitors, and Rheb siRNA were transfected to alter the expression of miR-155 and Rheb. Infarct sizes were measured using magnetic resonance imaging (MRI) and triphenyltetrazolium chloride (TTC) staining; cell apoptosis rates were calculated using Annexin V-FITC/PI staining and flow cytometry. Levels of miR-155, Rheb, mTOR, and S6K were examined by RT-PCR, immunofluorescence, and western blot. We performed a luciferase activity assay so that the association between miR-155 and Rheb could be fully assessed. RESULTS We demonstrated that miR-155 bound the 3'-UTR of Rheb and suppressed Rheb expression. As suggested by animal models, significant cerebral infarct volumes and cell apoptosis were induced by increased expression of miR-155 and decreased expression of Rheb, mTOR, and p-S6K (P<0.05). miR-155 inhibitors exhibited protective effects on ischemic stroke, including down-regulation of infarction size in cerebral tissues in vivo and reduced apoptosis of BV2 cells in vitro with increased expression of Rheb, mTOR and p-S6K (P<0.05). These protective effects could be substantially antagonized by the transfection of Rheb siRNA (P<0.05). CONCLUSIONS Inhibition of miR-155 may play protective roles in ischemic stroke by phosphorylating S6K through the Rheb/mTOR pathway.

Indexed as

Signal Transduction3' Untranslated RegionsAnimalsApoptosisBase SequenceBinding SitesBrainBrain IschemiaCell LineDisease Models, AnimalFlow CytometryImmunohistochemistryLuciferasesMagnetic Resonance ImagingMiceMicroRNAs3' Untranslated RegionsLuciferasesMicroRNAsMIRN155 microRNA, ratMonomeric GTP-Binding ProteinsNeuropeptidesRas Homolog Enriched in Brain ProteinRheb protein, ratRibosomal Protein S6 Kinases, 90-kDaTOR Serine-Threonine Kinases

Identifiers

PMID28025572
PMCPMC5215517
OpenAlexW2563235167

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.