This study examined the effect of over-expression of sFlt-1 by trophoblasts on the barrier function of glomerular endothelial cells and the role of VEGF in this process in order to explore the pathogenesis of glomerul...This study examined the effect of over-expression of sFlt-1 by trophoblasts on the barrier function of glomerular endothelial cells and the role of VEGF in this process in order to explore the pathogenesis of glomerular disease in preeclampsia. SFlt-1 expression in the human trophoblasts （TEV-1 cells） was enhanced by transfecting sFlt-1 plasmid DNA into TEV-1 cells. The monolayer barrier fimction of glomerular endothelial cells （ciGEnCs） was determined by measuring the fluorescence intensity of bovine serum albumin （BSA） that crossed the monolayer of glomerular endothelial cells. The results showed that the over-expression of sFlt-1 by TEV-1 cells led to the barrier dysfunction of ciGEnCs, and the exogenous VEGF could alleviate the ciGEnCs dysfunction resulting from the over-expression of sFlt- 1 to a certain extent. It was concluded that the dysregulation of sFlt- 1 and VEGF in preeclamptic pregnancy may contribute to the barrier dysfunction of glomerular endothelial cells, and VEGF may play an important role in maintaining the barrier function of glomerular endothelial cells, but it may not be the sole factor.展开更多
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 ...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.展开更多
Diabetic nephropathy is one of the most common causes of end-stage renal disease worldwide and is associated with increased mortality in patients with type 1 and type 2 diabetes.Autophagy is a highly conserved"au...Diabetic nephropathy is one of the most common causes of end-stage renal disease worldwide and is associated with increased mortality in patients with type 1 and type 2 diabetes.Autophagy is a highly conserved"autophagy"pathway and is an important mechanism for maintaining glomerular and tubular homeostasis.Emerging evidence suggests that targeted autophagy pathway activation and restoration of autophagy activity may have renal protection.Glomerular endothelial cells are an important key factor in the development of diabetic nephropathy.Endothelial dysfunction is involved in the development of diabetic and non-diabetic glomerular injury and renal fibrosis.Evidence of glomerular endothelial dysfunction in the late stages of diabetic nephropathy,such as thrombotic microangiopathy,including impairment of glomerular capillary microaneurysms and glomerular membrane lysis autophagy,is related to the pathogenesis of diabetic nephropathy.Here,we mainly introduced the research progress of the effects of glomerular endothelial cell autophagy on diabetic nephropathy.展开更多
文摘This study examined the effect of over-expression of sFlt-1 by trophoblasts on the barrier function of glomerular endothelial cells and the role of VEGF in this process in order to explore the pathogenesis of glomerular disease in preeclampsia. SFlt-1 expression in the human trophoblasts （TEV-1 cells） was enhanced by transfecting sFlt-1 plasmid DNA into TEV-1 cells. The monolayer barrier fimction of glomerular endothelial cells （ciGEnCs） was determined by measuring the fluorescence intensity of bovine serum albumin （BSA） that crossed the monolayer of glomerular endothelial cells. The results showed that the over-expression of sFlt-1 by TEV-1 cells led to the barrier dysfunction of ciGEnCs, and the exogenous VEGF could alleviate the ciGEnCs dysfunction resulting from the over-expression of sFlt- 1 to a certain extent. It was concluded that the dysregulation of sFlt- 1 and VEGF in preeclamptic pregnancy may contribute to the barrier dysfunction of glomerular endothelial cells, and VEGF may play an important role in maintaining the barrier function of glomerular endothelial cells, but it may not be the sole factor.
基金supported by a grant from Doctoral Program of Higher Education Research Fund Project (No.2010014 2110074)
文摘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.
文摘Diabetic nephropathy is one of the most common causes of end-stage renal disease worldwide and is associated with increased mortality in patients with type 1 and type 2 diabetes.Autophagy is a highly conserved"autophagy"pathway and is an important mechanism for maintaining glomerular and tubular homeostasis.Emerging evidence suggests that targeted autophagy pathway activation and restoration of autophagy activity may have renal protection.Glomerular endothelial cells are an important key factor in the development of diabetic nephropathy.Endothelial dysfunction is involved in the development of diabetic and non-diabetic glomerular injury and renal fibrosis.Evidence of glomerular endothelial dysfunction in the late stages of diabetic nephropathy,such as thrombotic microangiopathy,including impairment of glomerular capillary microaneurysms and glomerular membrane lysis autophagy,is related to the pathogenesis of diabetic nephropathy.Here,we mainly introduced the research progress of the effects of glomerular endothelial cell autophagy on diabetic nephropathy.
