Evidence map›Paper›PMID 20840605›Full record

ArticleThe FEBS journal2010

MicroRNA-21 protects neurons from ischemic death.

Ben Buller, Xianshuang Liu, Xinli Wang, Rui L Zhang, Li Zhang, Ann Hozeska-Solgot, Michael Chopp, Zheng G Zhang

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The FEBS journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed, 3 pooled it
5.4field-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

143 citing papers in PubMed, 3 syntheses or guidelines pooled it, 239 citations in OpenAlex.

  1. Pooled it
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  15. Article
  16. MicroRNA Profiles in Critically Ill Patients.Current medicinal chemistry · 2024
    Review
  17. Review
  18. Article
  19. Annals of translational medicine · 2023
    Article
  20. Review

83 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Ben BullerDepartment of Neurology, Henry Ford Hospital, Detroit, MI, USA.
Xianshuang Liu
Xinli Wang
Rui L Zhang
Li Zhang
Ann Hozeska-Solgot
Michael Chopp
Zheng G Zhang
Henry Ford Hospital · USOakland University · US

Funding

Treatment of Traumatic Brain Injury with Marrow Stromal CellsP01NS042345 · NINDS · HENRY FORD HEALTH SYSTEM · PI ZHANG, ZHENG GANG · 2003 to 2007
$6.1M
Treatment of Acute Embolic Stroke with Statins and rt-PAR01HL064766 · NHLBI · HENRY FORD HEALTH SYSTEM · PI ZHANG, ZHENG GANG · 2001 to 2009
$2.4M
Treatment of stroke with a clinically approved proteasome inhibitorR01NS062832 · NINDS · HENRY FORD HEALTH SYSTEM · PI ZHANG, LI · 2008 to 2012
$1.4M
NHLBI NIH HHS R01 HL064766NHLBI NIH HHS R01 HL64766NINDS NIH HHS P01 NS042345NINDS NIH HHS P01 NS42345NINDS NIH HHS R01 NS062832
6 · The paper itself

Abstract

MicroRNAs are small RNAs that attenuate protein expression by complementary binding to the 3'-UTR of a target mRNA. Currently, very little is known about microRNAs after cerebral ischemia. In particular, microRNA-21 (miR-21) is a strong antiapoptotic factor in some biological systems. We investigated the role of miR-21 after stroke in the rat. We employed in situ hybridization and laser capture microdissection in combination with real-time RT-PCR to investigate the expression of miR-21 after stroke. In situ hybridization revealed that miR-21 expression was upregulated in neurons of the ischemic boundary zone, and quantitative real-time RT-PCR analysis revealed that stroke increased mature miR-21 levels by approximately threefold in neurons isolated from the ischemic boundary zone by laser capture microdissection as compared with homologous contralateral neurons 2 days (n = 4; P < 0.05) and 7 days (n = 3; P < 0.05) after stroke. In vitro, overexpression of miR-21 in cultured cortical neurons substantially suppressed oxygen and glucose deprivation-induced apoptotic cell death, whereas attenuation of endogenous miR-21 by antisense inhibition exacerbated cell death after oxygen and glucose deprivation. Moreover, overexpression of miR-21 in neurons significantly reduced FASLG levels, and introduction of an miR-21 mimic into 293-HEK cells substantially reduced luciferase activity in a reporter system containing the 3'-UTR of Faslg. Our data indicate that overexpression of miR-21 protects against ischemic neuronal death, and that downregulation of FASLG, a tumor necrosis factor-α family member and an important cell death-inducing ligand whose gene is targeted by miR-21, probably mediates the neuroprotective effect. These novel findings suggest that miR-21 may be an attractive therapeutic molecule for treatment of stroke.

Indexed as

AnimalsCell DeathFas Ligand ProteinGene Expression RegulationIschemiaMicroRNAsNeuronsProtective AgentsRatsRats, WistarStrokeFaslg protein, ratFas Ligand ProteinMicroRNAsmirn21 microRNA, ratProtective Agents

Identifiers

PMID20840605
PMCPMC2957309
OpenAlexW1557444671

What OpenQuestion holds

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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.