Deregulation of MicroRNA‑31a‑5p is Involved in the Development of Primary Hypertension by Suppressing Apoptosis of Pulmonary Artery Smooth Muscle Cells Via Targeting TP53

The present study aimed to identify the association between microRNA (miRNA/miR)‑31a‑5p and the development of hypertension, and its potential molecular mechanism. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analyses were performed to validate the candidate miRNA and genes involved in hypertension, following which an online miRNA database search, luciferase assay, and RT‑qPCR and western blot analyses were performed to confirm the interaction between miR‑31a‑5p and TP53. A MTT assay and flow cytometric analysis were utilized to determine the effect of miR‑31a‑5p on cell growth and apoptosis. The results revealed that miR‑31a‑5p and TP53 were the candidate miRNA and gene regulating hypertension, and that TP53 was the virtual target gene of miR‑31a‑5p with a binding site located in the TP53 3' untranslated region (3'UTR). It was confirmed by luciferase activity that miR‑31a‑5p markedly reduced the luciferase activity of the Luc‑wild‑type‑TP53‑3'UTR, whereas the mutated putative miR‑31a‑5p binding located on the TP53‑3'UTR was found to eliminate such an inhibitory effect. miR‑31a‑5p had no effect on specificity protein 1, E2F transcription factor 2 or forkhead box P3 luciferase activity. Smooth muscle cells collected from spontaneously hypertensive rats treated with gold nano‑particles containing anti‑rno‑miR‑31a‑5p exhibited a lower growth rate and a higher apoptotic rate. The results of the RT‑qPCR and western blot analyses showed that miR‑31a‑5p negatively regulated the expression of TP53, and transfection with the hsa‑miR‑31a‑5p mimic significantly promoted cell growth and inhibited cell apoptosis, whereas transfection with the anti‑hsa‑miR‑31a‑5p mimic significantly suppressed cell growth and induced cell apoptosis. Taken together, these findings indicated that miR‑31a‑5p is involved in hypertension via the accelerated proliferation of arterial smooth muscle cells and inhibition of apoptosis through targeting TP53.