RGD Reference Report - MicroRNA-143 Increases Oxidative Stress and Myocardial Cell Apoptosis in a Mouse Model of Doxorubicin-Induced Cardiac Toxicity. - Rat Genome Database

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MicroRNA-143 Increases Oxidative Stress and Myocardial Cell Apoptosis in a Mouse Model of Doxorubicin-Induced Cardiac Toxicity.

Authors: Li, Xin-Qiang  Liu, Ya-Kui  Yi, Jun  Dong, Jia-Shou  Zhang, Pan-Pan  Wan, Lei  Li, Kui 
Citation: Li XQ, etal., Med Sci Monit. 2020 Mar 14;26:e920394. doi: 10.12659/MSM.920394.
RGD ID: 155883163
Pubmed: PMID:32170053   (View Abstract at PubMed)
PMCID: PMC7085239   (View Article at PubMed Central)
DOI: DOI:10.12659/MSM.920394   (Journal Full-text)

BACKGROUND Oxidative stress and myocardial apoptosis are features of doxorubicin-induced cardiac toxicity that can result in cardiac dysfunction. Previous studies showed that microRNA-143 (miR-143) was expressed in the myocardium and had a role in cardiac function. This study aimed to investigate the effects and possible molecular mechanisms of miR-143 on oxidative stress and myocardial cell apoptosis in a mouse model of doxorubicin-induced cardiac toxicity. MATERIAL AND METHODS Mice underwent intraperitoneal injection of doxorubicin (15 mg/kg) daily for eight days to develop the mouse model of doxorubicin-induced cardiac toxicity. Four days before doxorubicin administration, a group of mice was pretreated daily with a miR-143 antagonist (25 mg/kg/day) for four consecutive days by tail vein injection. The study included the use of a miR-143 antagomir, or anti-microRNA, an oligonucleotide that silenced endogenous microRNA (miR), and an agomir to miR-143, and also the AKT inhibitor, MK2206. Quantitative real-time polymerase chain reaction (qRT-PCR) and immunoblot analysis were used to measure mRNA and protein expression, respectively. RESULTS Doxorubicin treatment increased the expression of miR-143, which was reduced by the miR-143 antagomir. Overexpression of miR-143 increased doxorubicin-induced myocardial apoptosis and oxidative stress. The use of the miR-143 antagomir significantly activated protein kinase B (PKB) and AKT, which were reduced in the presence of the AKT inhibitor, MK2206. However, the use of the miR-143 antagomir further down-regulated AKT phosphorylation following doxorubicin treatment and increased AKT activation. CONCLUSIONS In a mouse model of doxorubicin-induced cardiac toxicity, miR-143 increased oxidative stress and myocardial cell apoptosis following doxorubicin treatment by inhibiting AKT.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Cardiotoxicity amelioratesISOMir143 (Mus musculus)155883163; 155883163 RGD 
Cardiotoxicity amelioratesIMP 155883163 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Mir143  (microRNA 143)

Genes (Mus musculus)
Mir143  (microRNA 143)

Genes (Homo sapiens)
MIR143  (microRNA 143)


Additional Information