ΜicroRNA-221 participates in cerebral ischemic stroke by modulating endothelial cell function by regulating the PTEN/PI3K/AKT pathway

An effective method to improve the blood supply of brain tissue is by angiogenesis, which is crucial for the prognosis of patients with cerebral ischemic stroke (CIS). Therefore, angiogenesis has been a focus of CIS research in recent years. The present study aimed to investigate the expression of microRNA (miR)-221 in patients with CIS and to explore the effect of miR-221 on endothelial cell function. The level of miR-221 was detected using reverse transcription-quantitative PCR (RT-qPCR). The relationship between miR-221 and phosphatase and tensin homolog (PTEN) was predicted and confirmed by bioinformatics and dual luciferase reporter assay. Cell viability, migration and invasion, and cell apoptosis were determined using MTT assay, Transwell assay and flow cytometry respectively. Tube formation in human umbilical vein endothelial cells (HUVECs) was determined by performing the tube formation assay. In addition, protein levels were measured using western blot analysis. The results of the current study indicated that miR-221 levels were significantly decreased in the peripheral blood of patients with CIS. PTEN was confirmed to be a direct target of miR-221. Downregulation of miR-221 significantly inhibited the function of HUVECs as evidenced by the decreased cell viability, migration and invasion with increased cell apoptosis and tube formation inhibition. miR-221 upregulation produced the reverse effects, whilst all the effects of miR-221 upregulation on HUVECs were reversed by PTEN overexpression. The PI3K/AKT pathway was identified to be involved in the regulation of miR-221 on HUVECs. In conclusion, miR-221 was downregulated in CIS patients, and it promoted the function of HUVECs by regulating the PTEN/PI3K/AKT pathway in vitro, suggesting the ability to promote angiogenesis. Therefore, miR-221 may be a novel and promising therapeutic target for CIS treatment.