Downregulated microRNA‑133a induces HUVECs injury: Potential role of the (pro) renin receptor in angiotensin II‑dependent hypertension.

The renin‑angiotensin system (RAS) serves an essential role in hypertension. MicroRNAs (miRs) have been reported to be important regulators in angiotensin (Ang) II‑dependent hypertension. We aimed to explore the roles of Ang II and miR‑133a in the mechanism underlying hypertension. Human umbilical vein endothelial cells (HUVECs) were identified by immunofluorescence staining. Cell viability and miR‑133a expression under the inhibition of Ang II of various concentrations were determined by an MTT assay and reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), respectively. The effects of HUVECs transfected with miR‑133a mimic or inhibitor on Ang II‑induced apoptosis were measured using flow cytometry. The potential targeting of miR‑133a to the 3' untranslated region of (pro) renin receptor (PRR) was assessed using TargetScan and a dual‑luciferase assay. The effects of PRR interference using small interfering (si)RNA on PRR expression and the rate of apoptosis were determined by RT‑qPCR, western blotting and flow cytometry, respectively. Ang II at a concentration of 10‑5 M significantly inhibited the cell viability (P<0.05) and miR‑133a expression (P<0.01); Downregulation of miR‑133a suppressed cell viability. HUVECs transfected with miR‑133a mimic reduced the rate of Ang II‑induced apoptosis from 21.99 to 12.38%, but miR‑133a inhibitor promoted Ang II‑induced apoptosis (apoptosis rate, 28.9%). PRR was predicted to be a target gene of miR‑133a. Transfection with siPRR decreased the apoptotic rate in Ang II + negative control and Ang II + miR‑133a inhibitor group to 11.39 and 12.94%, respectively. Our findings also suggested that Ang II promoted PRR expression to enhance the apoptotic rate of HUVECs via the suppression of miR‑133a. Furthermore, siPRR efficiently decreased the Ang II‑induced apoptosis.