Abstract
Aortic dissection (AD) is one of the most lethal cardiovascular diseases. Endothelial cell (EC) dysfunction serves an important role in AD progression. Angiotensin II (Ang II) is a key effector in cardiovascular disease development that acts through binding to angiotensin type 1 receptor (AT1R). Yes-associated protein (YAP) is well-known as a key mediator of cell proliferation and apoptosis. To determine whether AT1R and YAP influence EC proliferation or injury, human aortic endothelial cells were cultured under different culture conditions. Using CCK-8 assay, ELISA, western blotting, immunocytochemistry and siRNA transfection, the present study found that Ang II activity reduced EC proliferation, upregulate YAP phosphorylation and result in EC injury that was associated with elevated levels of multiple proinflammatory chemokines. The inhibition of AT1R function, pharmaceutically or via transfection with an AT1R small interfering RNA, alleviated the effects induced by Ang II. Furthermore, AT1R induced YAP phosphorylation via binding to Ang II, and further promoted the inflammation of ECs, along with inhibiting their proliferation.