Abstract
Acute cerebral infarction (ACI) is a common cerebrovascular disease. Previous studies have indicated that microRNAs (miRs) are aberrantly expressed in patients with ACI. However, the functions of miRs in the pathogenesis of ACI still require further investigation. The aim of the present study was to investigate the function of miR-210 in ACI and its associated mechanism. The expression of miR-210 in the serum of 40 patients with ACI and 40 normal controls was examined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Then, human umbilical vein endothelial cells (HUVECs) were treated with serum from patients with ACI or healthy volunteers, and a CCK-8 assay was performed to examine cell proliferation. Next, cells were stained with PI/Annexin V, and the apoptosis rate was examined using flow cytometry. Furthermore, cells were harvested and lysed, and RT-qPCR and western blotting assays were performed to compare the expression of vascular endothelial growth factor (VEGF), Notch1 and Hes1 in different groups. It was observed that the expression of miR-210 was significantly increased in the serum of patients with ACI compared with normal controls (P<0.01), and receiver operating characteristic curve analysis indicated that the area under the curve for miR-210 was 0.799 (95% confidence interval, 0.700-0.899), the optimum cut-off point was 1.397, and the sensitivity and specificity at the cut-off point were 62.5 and 87.5%, respectively. Furthermore, serum from patients with ACI induced a significant increase in proliferation (P<0.05 at 48 h, P<0.01 at 72 h) and a significant decrease in the apoptosis rate of HUVECs (P<0.01). In addition, serum from patients with ACI significantly increased the expression of VEGF, Notch1 and Hes1 at the mRNA and protein level (all P<0.01 with the exception of Notch1 mRNA expression, P>0.05). In conclusion, these results demonstrate that miR-210 is upregulated in the serum of patients with ACI, and miR-210 may be involved in the pathogenesis of ACI through regulating the proliferation and apoptosis of endothelial cells.