miR-29a regulates VSMC cell proliferation and its roles in the pathogenesis of hypertension through targeting PTEN

Vascular smooth muscle cell (VSMC) hyperplasia is related to hypertension. Phosphatase and tensin homology deleted on chromosome ten (PTEN) is the inhibitor of PI3K/AKT signaling pathways. Bioinformatics analysis has demonstrated the targeting relationship between miR-29a and PTEN mRNA 3'-UTR. The current study investigated the roles of miR-29a in regulating PTEN expression, VSMC proliferation, and the pathogenesis of hypertension. miR-29a, PTEN, p-AKT, and Ki67 expression in the media of SHR and WKY rats was compared. The targeted relationship between miR-29a and PTEN was confirmed by dual luciferase reporter assay. SHR rats were randomly divided into two groups, antagomir-29a and antagomir-NC groups. Systolic blood pressure (SBP) and diastolic pressure (DBP) of the caudal arteries were compared. PTEN and p-AKT expression in the blood vessels was detected by Western blot. VSMCs were cultured in vitro and divided into two transfection groups, the miR-NC group and miR-29a inhibitor group. Cell proliferation was tested by EdU staining. Compared with WKY rats, miR-29a, p-AKT, and Ki67 expression was significantly increased, while PTEN levels were obviously declined in the vascular media of SHR rats. In vivo injections of antagomir-29a upregulated PTEN expression, reduced p-AKT and Ki67 levels, and decreased systolic and diastolic blood pressure in the vascular tissue of rats. Transfection of miR-29a markedly enhanced PTEN expression, decreased p-AKT expression, and weakened cell proliferation in VSMC cells in vitro. miR-29a plays a role in lowering blood pressure by inhibiting PTEN, enhancing the activity of PI3K/AKT signaling pathways, and suppressing VSMC cell proliferation.