The Molecular Mechanism of the Proliferation of Human Umbilical Vein Endothelial Cells Induced by Angiolensin II

Objective: To explore the molecular mechanism of the proliferation of human umbilical vein endothelial cells induced by AngⅡ.Methods: The lines of human umbilical vein endothelial cell cultured in vitro were divided into 3 groups which were treated by AngⅡ, AngⅡ+NAC, and normal culture medium respectively. First we observed the proliferous effect of human umbilical vein endothelial cells induced by AngⅡ at different concentration at different time with biochemical methods. Then the contents of ROS(·OH) in 3 groups were detected by spectrophotometer. Finally we detected the related gene expression in the process of human umbilical vein endothelial cells proliferation via the technique of genechips.Results: Human umbilical vein endothelial cells incubated with AngⅡ(0.03125～1μmol/L ) for 12 hours increased the proliferation rate (P0.05);the negative correlation between proliferation rate and the contents of ROS(·OH)(r=-0.8, P0.01) was significant;NAC can reduce the content of ROS(·OH) and inhibit the proliferation of human umbilical vein endothelial cells;The technique of genechips analysis suggests that the genes expression related to proliferation such as ERK, Akt, CCN and PCNA increased, while the gene expression related to apoptosis such as DR6, Caspases6 BAK1 and PDCD8 decreased when human umbilical vein endothelial cell were induced by AngⅡ(0.0625μmol/L) for 12 hours; In contrast, when human umbilical vein endothelial cells were induced by AngⅡ(1μmol/L) for 12 hours, we can obtain reverse results. Conclusion: Human umbilical vein endothelial cells induced by AngⅡcan produce ROS(·OH).The target gene expression related to proliferation of human umbilical vein endothelial cells may be mediated by ROS(·OH), ROS(·OH) may be the molecules which play an important role in the signal transduction and gene expression of proliferation.