Abstract | BACKGROUND:
MicroRNAs play important roles in regulation of the cardiovascular system. The purpose of this study was to investigate microRNA-320 (miR-320) expression in myocardial ischemia-reperfusion (I/R) injury and the roles of miR-320 in cardiomyocyte apoptosis by targeting AKIP1 (A kinase interacting protein 1). METHODS: The level of miR-320 was detected using quantitative real-time polymerase chain reaction (qRT-PCR), and cardiomyocyte apoptosis was detected via terminal dUTP nick end-labeling assay. Cardiomyocyte apoptosis and the mitochondrial membrane potential were evaluated via flow cytometry. Bioinformatics tools were used to identify the target gene of miR-320. The expression levels of AKIP1 mRNA and protein were detected via qRT-PCR and Western blot, respectively. RESULTS: Both the level of miR-320 and the rate of cardiomyocyte apoptosis were substantially higher in the I/R group and H9c2 cells subjected to H/R than in the corresponding controls. Overexpression of miR-320 significantly promoted cardiomyocyte apoptosis and increased the loss of the mitochondrial membrane potential, whereas downregulation of miR-320 had an opposite effect. Luciferase reporter assay showed that miR-320 directly targets AKIP1. Moreover, knock down and overexpression of AKIP1 had similar effects on the H9c2 cells subjected to H/R. CONCLUSIONS: miR-320 plays an important role in regulating cardiomyocyte apoptosis induced by I/R injury by targeting AKIP1 and inducing the mitochondrial apoptotic pathway.
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Authors | Zhi-Qiang Tian, Hong Jiang, Zhi-Bing Lu |
Journal | Cellular & molecular biology letters
(Cell Mol Biol Lett)
Vol. 23
Pg. 41
( 2018)
ISSN: 1689-1392 [Electronic] England |
PMID | 30181740
(Publication Type: Journal Article)
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Chemical References |
- AKIP1 protein, mouse
- AKIP1 protein, rat
- Adaptor Proteins, Signal Transducing
- MIRN320 microRNA, rat
- MicroRNAs
- Mirn320 microRNA, mouse
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Topics |
- Adaptor Proteins, Signal Transducing
(genetics)
- Animals
- Apoptosis
- Cell Line
- Gene Expression Regulation
- Male
- Mice, Inbred C57BL
- MicroRNAs
(genetics)
- Myocardial Reperfusion Injury
(genetics, pathology)
- Myocytes, Cardiac
(metabolism, pathology)
- Rats
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