RGD Reference Report - MicroRNA-21 protects neurons from ischemic death. - Rat Genome Database

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MicroRNA-21 protects neurons from ischemic death.

Authors: Buller, Ben  Liu, Xianshuang  Wang, Xinli  Zhang, Rui L  Zhang, Li  Hozeska-Solgot, Ann  Chopp, Michael  Zhang, Zheng G 
Citation: Buller B, etal., FEBS J. 2010 Oct;277(20):4299-307. doi: 10.1111/j.1742-4658.2010.07818.x. Epub 2010 Sep 14.
RGD ID: 41410884
Pubmed: PMID:20840605   (View Abstract at PubMed)
PMCID: PMC2957309   (View Article at PubMed Central)
DOI: DOI:10.1111/j.1742-4658.2010.07818.x   (Journal Full-text)

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.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
cerebral infarction  ISOMir21 (Rattus norvegicus)41410884; 41410884RNA:increased expression:brainRGD 
cerebral infarction  IEP 41410884RNA:increased expression:brainRGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
negative regulation of neuron apoptotic process  IMP 41410884 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Mir21  (microRNA 21)

Genes (Mus musculus)
Mir21a  (microRNA 21a)

Genes (Homo sapiens)
MIR21  (microRNA 21)


Additional Information