RGD Reference Report - Down-regulation of miR-320 exerts protective effects on myocardial I-R injury via facilitating Nrf2 expression. - Rat Genome Database

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Down-regulation of miR-320 exerts protective effects on myocardial I-R injury via facilitating Nrf2 expression.

Authors: Zhu, X-A  Gao, L-F  Zhang, Z-G  Xiang, D-K 
Citation: Zhu XA, etal., Eur Rev Med Pharmacol Sci. 2019 Feb;23(4):1730-1741. doi: 10.26355/eurrev_201902_17135.
RGD ID: 155882546
Pubmed: PMID:30840298   (View Abstract at PubMed)
DOI: DOI:10.26355/eurrev_201902_17135   (Journal Full-text)


OBJECTIVE: Nuclear factor NF-E2 related factor 2 (Nrf2) plays crucial roles in the regulation of oxidative stress (OS) or myocardial ischemia-reperfusion (I-R) injury. During the process of I-R injury, the miR-320 is down-regulated. Bioinformatics analysis showed complementary binding sites between miR-320 and 3'-UTR of Nrf2 mRNA. Therefore, this study aimed to investigate the role of miR-320 in mediating Nrf2 expression and myocardial I-R injury.
MATERIALS AND METHODS: Rat I-R model was established. Fluorescent quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot were used to measure the expression of miR-320, Nrf2, HO-1 in myocardial tissues. Contents of malondialdehyde (MDA), superoxide dismutase (SOD) and caspase-3 activity, serum assay of creatine kinase (CK) and lactate dehydrogenase (LDH) activity were evaluated. I-R rat models were transfected with antagomir-320 followed by measuring those proteins. Cultured H9C2 cells were transfected with antagomir-320 to measure miR-320, Nrf2 and heme oxygenase 1 (HO-1) expression, cell apoptosis and reactive oxygen species (ROS) content.
RESULTS: Compared to the sham group, I-R rats had significantly lower miR-320 or HO-1 expression in the myocardium, plus higher levels of Nrf2, MDA, CK and LDH, and decreased SOD activity (p<0.05). Antagomir-320 transfection suppressed miR-320 expression, elevated Nrf2 and HO-1 expression, decreased levels of MDA, CK or LDH, and increased SOD activity. In H9C2 cells, antagomir-320 transfection also elevated Nrf2 and HO-1 expression and suppressed myocardial cell apoptosis or ROS production under I-R treatment.
CONCLUSIONS: Down-regulation of miR-320 exerts protective effects on myocardial I-R injury. The inhibition of mir-320 expression can enhance OS potency of the myocardium, alleviate I-R injury or reduce cell apoptosis by facilitating Nrf2 expression.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Myocardial Reperfusion Injury treatmentISOMir320a (Rattus norvegicus)155882546; 155882546 RGD 
Myocardial Reperfusion Injury treatmentIMP 155882546 RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
positive regulation of cardiac muscle cell apoptotic process  IMP 155882546 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Mir320a  (microRNA 320a)

Genes (Mus musculus)
Mir320  (microRNA 320)

Genes (Homo sapiens)
MIR320A  (microRNA 320a)


Additional Information