Purpose: Myocardial infarction is a common cardiovascular disease. MicroRNA-16-5p
(miR-16-5p) was upregulated in heart and kidney hypoxia/reoxygenation (H/R) injury. However,
the role of miR-16-5p in myocardial infarction injury is still unclear.
Methods: Human adult ventricular cardiomyocytes (AC16) were treated with ischemia/reperfusion
(H/R). The miR-16-5p level was evaluated through real-time PCR. The activity of lactate dehydrogenase
(LDH) and creatine kinase-MB (CK-MB) was detected via LDH and CK-MB monitoring
kits. Cell viability was examined with 3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetra-zolium
bromide (MTT) assay. Western blotting was used to analyze the protein levels. The luci-ferase report
assay confirmed the relative luciferase activity.
Results: miR-16-5p was elevated in H/R-treated AC16 cells. miR-16-5p overexpression and
knockdown were carried out. miR-16-5p knockdown repressed cell apoptosis, attenuated LDH and
CK-MB activities, and enhanced cell viability in H/R-treated AC16 cells. Moreover, miR-16-5p
knockdown promoted angiogenesis in human microvascular endothelial cells (HMVEC), causing
elevation of vascular endothelial growth factor (VEGF), insulin receptor substrates 1 (IRS1),
minichromosome maintenance complex component 2 (MCM2) and proliferating cell nuclear antigen
(PCNA) protein levels. Moreover, miR-16-5p was testified to target IRS1. IRS1 silencing
alleviated miR-16-5p knockdown-mediated inhibition of apoptosis in AC16 cells.
Conclusion: miR-16-5p knockdown increased cell viability and angiogenesis, as well as inhibited
cell apoptosis by increasing IRS1. These findings indicated that miR-16-5p knockdown may be a
new therapeutic target for myocardial infarction.