MicroRNA-144 attenuates cardiac ischemia/reperfusion injury by targeting FOXO1
Autor: | Hong Jiang, Lusha E, Zhibing Lu |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Cancer Research FOXO1 03 medical and health sciences 0302 clinical medicine Immunology and Microbiology (miscellaneous) microRNA medicine myocardium Oncogene business.industry microRNA-144 General Medicine Articles Hypoxia (medical) medicine.disease Molecular medicine ischemia/reperfusion forkhead box protein O1 030104 developmental biology Real-time polymerase chain reaction Apoptosis 030220 oncology & carcinogenesis Cancer research medicine.symptom business Corrigendum Reperfusion injury |
Zdroj: | Experimental and Therapeutic Medicine |
ISSN: | 1792-0981 |
Popis: | Cardiovascular ischemic disease refers to a large class of conditions that are harmful to human health. A number of previous studies have demonstrated that microRNAs (miRs) have notable roles in regulating cardiac injury. miR-144 is influential in the differentiation, growth, and metastatic processes of cells; however, the impact of miR-144 in cardiac ischemia/reperfusion (I/R) injury has not been thoroughly elucidated to date. In the present study, reverse transcription quantitative polymerase chain reaction was used to evaluate RNA expression. In addition, TTC staining was performed to detect the infarct area of the ischemic myocardia and a terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assay was utilized to detect the apoptosis of the myocardia. It was observed that miR-144 expression is downregulated in an I/R model in rats and that overexpression of miR-144 significantly reduced myocardial ischemic injury and apoptosis. Consistent with this result, similar findings were demonstrated in H9c2 cells subjected to hypoxia/reoxygenation. Bioinformatic analysis using MiRanda and TargetScan, and luciferase assays confirmed that forkhead box protein O1was the target of miR-144. These findings suggest that miR-144 may be exploited as a novel molecular marker or therapeutic target for myocardial I/R injury. |
Databáze: | OpenAIRE |
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