MicroRNA-510-3p alleviates endothelial dysfunction in a DOCA-salt rat model of hypertension by targeting phosphatase and tensin homolog and its signaling axis.

Essential hypertension, characterized by persistent elevation of blood pressure, is often associated with endothelial dysfunction (ED), marked by impaired endothelial activity. Despite advancements, the molecular mechanisms underlying ED in hypertension remain unclear. This study aimed to investigate the role of microRNA-510-3p (miR-510-3p) in regulating endothelial function through the PTEN/PI3K/AKT/eNOS signaling pathway and to evaluate its potential as a biomarker and potential therapeutic target for DOCA-salt-induced experimental hypertension. Bioinformatic and luciferase analysis suggest PTEN as a potential direct target of miR-510-3p. Human umbilical vein endothelial cells (HUVECs) were employed to assess proliferation, migration, apoptosis, and dual-luciferase activity. The expression levels of miR-510-3p, PTEN, PI3K, AKT, and eNOS were quantified using qRT-PCR in both HUVECs and rat tissues. Hypertensive DOCA-salt-induced rats exhibited significantly increased systolic and diastolic pressures with evident vascular hypertrophy. Both mRNA expression analyses revealed elevated miR-510-3p, PI3K, AKT, and eNOS levels and a marked decrease in PTEN expression in HUVECs and hypertensive DOCA-salt-induced rats. miR-510-3p is associated with changes in endothelial function and PTEN expression, potentially involving the PI3K/AKT/eNOS signaling pathway. Taken together, miR-510-3p may represent a candidate biomarker and potential therapeutic target, warranting further validation. However, as the DOCA-salt model primarily reflects a low-renin, volume-dependent form of hypertension, these findings may not fully represent the complexity of human essential hypertension.