The Effect of MicroRNA-101 on Angiogenesis of Human Umbilical Vein Endothelial Cells during Hypoxia and in Mice with Myocardial Infarction

Abstract EN

Background.

Previous studies showed that recanalization and angiogenesis within the infarct region are of vital importance to the survival of myocardial cells during the treatment of acute myocardial infarction (AMI).

Methods.

In this study, EdU cell proliferation assay, Transwell assay, scratch wound assay, and tube formation assay were used.

Twelve bioinformatics analysis packages were used to predict the target genes of miR-101.

Target genes were verified by luciferase reporter generation and assay, fluorescent quantitative PCR, and western blotting.

Animal model and treatments were detected by M-mode echocardiography and immunofluorescent staining of CD31, Ki67, and α-SMA.

Results.

AgomiR-101 significantly enhanced HUVEC proliferation, migration, and tube formation.

A double-luciferase reporter assay revealed that the hsa-miR-101 mimic attenuated the activity of the EIF4E3′-UTR-wt type plasmid by 36%.

The expression levels of HIF-1α and VEGF-A in the scrambled RNA group were significantly lower than those in the EIF4E3 siRNA and agomiR-101 groups.

The left ventricular ejection fraction of the AMI+Adv-miR-101 group was significantly higher than that of the AMI+Adv-null and Sham+Adv-null groups.

The proliferation of vessel cells in the peripheral infarcted myocardium was higher in the AMI+Adv-miR-101 group than that in the AMI+Adv-null and Sham+Adv-null groups.

Conclusion.

MiR-101 can promote angiogenesis in the region surrounding the myocardial infarction.