miR-155 suppresses palmitic acid-induced vascular smooth muscle cell dysfunction by targeting angiotensin II type 1 receptor

miR-155 is a multifunctional post-translational modulator that participates in a variety of diseases. However, the relationship between palmitic acid (PA), miR-155 and AT1R has yet to be fully explored in cardiovascular diseases. In this study, we hypothesized that a post-translational mechanism of microRNAs regulated the expression of AT1R in PA-treated VSMCs. First, we found that PA could accelerate the mitochondrial dysfunction and DNA damage and induce VSMCs apoptosis in vitro. Next, abnormally expressed AT1R and miR-155 were simultaneously induced by PA in VSMCs. Intriguingly, bioinformatic analysis showed the potential miR-155 binding sites within the 3'-UTR of AT1R in human VSMCs. Luciferase assays verified significantly reduced luciferase activity in miR-155-transfected wild-type VSMCs compared with NC cells. In addition, miR-155 could inhibit PA-induced apoptosis and reverse PA-induced increase of AT1R in VSMCs. In conclusion, the results suggested that overexpressed miR-155 inhibited PA-induced VSMCs dysfunction, and the underlying mechanism was mediated, at least partially, through the suppression of AT1R expression.