VEGF deficit is involved in endothelium dysfunction in preeclampsia.

This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry, real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. VEGF expression in the human umbilical vein endothelial cells (HUVECs) was blocked by small interfering RNAs (siRNAs). The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers. The cell proliferation and cell-secreted nitric oxide (NO) level were detected by MTT method and nitrate reductase assay, respectively. The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue. The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects, although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high. Moreover, VEGF deficit could lead to endothelium cell dysfunction, and the administration of VEGF could protect endothelium cells from injury. It was concluded that lack of VEGF contributes to endothelium dysfunction, which may lead to the occurrence and development of preeclampsia.