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The mechanism of injury on the human glomerular endothelial cells(ciGENC) induced by preeclampsia serum was investigated.Concentration of maternal serum sFlt-1 protein was detected by ELISA.Fluorescently-labeled bovine serum albumin infiltrating through lower chamber of Transwell was measured by multifunction microplate reader.Morphologic change of ciGENC was observed under inverted phase contrast microscope.The concentration of sflt-1 in preeclampsia groups was significantly increased as compared with control group(P<0.01).Permeability in preeclampsia groups was significantly increased as compared with control group(P<0.01).By contrast with severe preeclampsia group,the permeability of ciGENC monolayer in mild preeclampsia group was decreased significantly(P<0.05).Intervention of exogenous VEGF significantly decreased permeability of ciGENC in preeclampsia groups.It was concluded that sFlt-1 increased ciGENC permeability by damaging integrity of endothelial barrier function.
The mechanism of injury on the human glomerular endothelial cells (cGen) induced by preeclampsia serum was investigated. Concentration of maternal serum sFlt-1 protein was detected by ELISA. Fluorescently-labeled bovine serum albumin infiltrating through lower chamber of Transwell was measured by multifunction microplate reader. Morphologic change of ciGENC was observed under inverted phase contrast microscope. The concentration of sflt-1 in preeclampsia groups was significantly increased compared to control group (P <0.01). Permeability in preeclampsia groups was significantly increased as compared with control group ( P <0.01) .By contrast with severe preeclampsia group, the permeability of ciGENC monolayer in mild preeclampsia group was decreased significantly (P <0.05) .Intervention of exogenous VEGF significantly decreased permeability of cGENC in preeclampsia groups. It was concluded that sFlt-1 increased ciGENC permeability by damaging integrity of endothelial barrier function.