Furthermore, an in vitro study on human umbilical vein endothelial cells revealed that PCs could contribute to endothelial dysfunction through the mechanism of increased endothelial permeability, along with reorganized presentation of endothelial actin and VE cadherin and inhibition of endothelial proliferation and wound repair in a dose-dependent manner [11,12]. This evidence concerns the gene CDH5 and endothelial dysfunction.