Abstract
Previous studies have indicated that microRNAs (miRNAs/miRs) may participate in the pathogenesis of hypertension. miR-145 has been demonstrated to serve important roles in the development of numerous cardiovascular diseases. However, the specific role of miR-145 in hypertension remains unclear. The present study aimed to investigate the role of miR-145 in spontaneously hypertensive rats (SHR) and rat vascular endothelial cells (RVECs). The results of the present study demonstrated that in the SHR group miR-145 expression was significantly upregulated in the thoracic aorta compared with the control group. Furthermore, a significant decrease in nitric oxide (NO) content was observed in the SHR group compared with the control rats. In RVECs, silencing miR-145 induced a significant increase in the expression of solute carrier family 7 member 1 (SLC7A1) and phosphorylated endothelial nitric oxide synthase, and a dual-luciferase reporter assay confirmed that SLC7A1 is a direct target of miR-145. The results of the present study indicate that miR-145 functions as a key mediator in the pathogenesis of hypertension via targeting SLC7A1, which suggests that miR-145 is a potential target for the treatment of hypertension.