Epidemiological studies suggest that the impact of preeclampsia not only on the mother but particularly on the children.We know that adverse events in utero may predispose to premature cardiovascular disease in adulthood, but we dont know the mechanisms.To gain insights into the mechanisms of cardiovascular dysfunction in offspring of preeclampsia, we employed a global stable isotope labeled profiling strategy using iTRAQ reagents, followed by 2D-LC-MS/MS.We identified 1521 non-redundant proteins, and 1496 of these were quantified.Further analysis identified 53 differentially expressed proteins in umbilical artery from preeclampsia; 22 proteins were up-regulated and 31 proteins were down-regulated.Hierarchical clustering analysis showed that the protein expression profile specific for umbilical artery can distinguish between normal and preeclampsia.These 53 proteins were analyzed by Ingenuity Pathway Analysis (IPA) software and were found to be played important roles in the angiogenesis, vasculogenesis and development of cardiovascular system.In addition, three differential expressions of cardiovascular relative proteins (Aldose reductase, Fibronectin-1, Fibrillin-1) were independently verified using western blot.These results may be supply a new sights into the mechanisms of vascular dysfunction of offspring from preeclampsia.