Evidence map›Paper›PMID 27980410›Full record

ArticleNeuropsychiatric disease and treatment2016

miR-455 inhibits neuronal cell death by targeting TRAF3 in cerebral ischemic stroke.

Shengtao Yao, Bo Tang, Gang Li, Ruiming Fan, Fang Cao

Open access · goldAbstract read
In one paragraph

Article in Neuropsychiatric disease and treatment, 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
2.2field-weighted citation impact, top 13% 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, 49 citations in OpenAlex.

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  14. Neurovascular Unit: A critical role in ischemic stroke.CNS neuroscience & therapeutics · 2021
    Review
  15. Review
  16. LncRNA promoted inflammatory response in ischemic heart failure through regulation of miR-455-3p/TRAF6 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
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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 1 institution in 1 country.

Shengtao YaoDepartment of Cerebrovascular Disease, The First Affiliated Hospital of Zunyi Medical College, Zunyi, People's Republic of China.
Bo TangDepartment of Cerebrovascular Disease, The First Affiliated Hospital of Zunyi Medical College, Zunyi, People's Republic of China.
Gang LiDepartment of Cerebrovascular Disease, The First Affiliated Hospital of Zunyi Medical College, Zunyi, People's Republic of China.
Ruiming FanDepartment of Cerebrovascular Disease, The First Affiliated Hospital of Zunyi Medical College, Zunyi, People's Republic of China.
Fang CaoDepartment of Cerebrovascular Disease, The First Affiliated Hospital of Zunyi Medical College, Zunyi, People's Republic of China.
Affiliated Hospital of Zunyi Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke is one of the leading causes of brain disease, with high morbidity, disability, and mortality. MicroRNAs (miRNAs) have been identified as vital gene regulators in various types of human diseases. Accumulating evidence has suggested that aberrant expression of miRNAs play critical roles in the pathologies of ischemic stroke. Yet, the precise mechanism by which miRNAs control cerebral ischemic stroke remains unclear. In the present study, we explored whether miR-455 suppresses neuronal death by targeting TRAF3 in cerebral ischemic stroke. The expression levels of miR-455 and TRAF3 were detected by quantitative real-time polymerase chain reaction and Western blot. The role of miR-455 in cell death caused by oxygen-glucose deprivation (OGD) was assessed using Cell Counting Kit-8 (CCK-8) assay. The influence of miR-455 on infarct volume was evaluated in mouse brain after middle cerebral artery occlusion (MCAO). Bioinformatics softwares and luciferase analysis were used to find and confirm the targets of miR-455. The results showed that the expression levels of miR-455 significantly decreased in primary neuronal cells subjected to OGD and mouse brain subjected to MCAO. In addition, forced expression of miR-455 inhibited neuronal death and weakened ischemic brain infarction in focal ischemia-stroked mice. Furthermore, TRAF3 was proved to be a direct target of miR-455, and miR-455 could negatively suppress TRAF3 expression. Biological function analysis showed that TRAF3 silencing displayed the neuroprotective effect in ischemic stroke and could enhance miR-455-induced positive impact on ischemic injury both in vitro and in vivo. Taken together, miR-455 played a vital role in protecting neuronal cells from death by downregulating TRAF3 protein expression. These findings may represent a novel latent therapeutic target for cerebral ischemic stroke.

Indexed as

cerebral ischemic strokeMCAOmiR-455neuronal cellTRAF3

Identifiers

PMID27980410
PMCPMC5147416
OpenAlexW2560334057

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.