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Abstract: FR-PO598

Endoglin Mediates Endothelial Activation and Monocyte Adhesion and Is Correlated with Glomerular VCAM-1 in Patients with Diabetic Nephropathy

Session Information

Category: Diabetes

  • 501 Diabetes Mellitus and Obesity: Basic - Experimental


  • Bus, Pascal, Leiden University Medical Center, Leiden, Netherlands
  • Gerrits, Tessa, LUMC, Leiden, Netherlands
  • Heemskerk, Sharon, LUMC, Leiden, Netherlands
  • Zandbergen, Malu, LUMC, Leiden, Netherlands
  • Bruijn, Jan A., Leiden University Medical Center, Dept.Pathology, Leiden, Netherlands
  • Baelde, Hans J., Leiden University Medical Center, Leiden, Netherlands
  • Scharpfenecker, Marion, Leiden University Medical Center, Leiden, Netherlands

Diabetic nephropathy is characterized by microvascular injury driven by hyperglycemia and enhanced growth factor production. Altered growth factor expression causes an angiogenic imbalance resulting in endothelial activation and dysfunction. Endothelial activation promotes the adhesion and subsequent infiltration of inflammatory cells, which promote renal damage in diabetic animal models. Endoglin is crucial for angiogenesis and vascular development, and is associated with endothelial activation and inflammation in animal models of renal disease. Here, we investigated whether reducing endothelial endoglin expression affects endothelial activation and monocyte adhesion under diabetic conditions in vitro, and we investigated which glomerular cells express endoglin and VCAM-1, and whether glomerular endoglin expression is associated with endothelial activation in patients with diabetic nephropathy.


Immortalized endothelial cells with either wild type or reduced endoglin expression were used to study endothelial activation and monocyte adhesion after stimulation with either glucose or VEGF-A. Glomerular endoglin and VCAM-1 expression was studied by immunohistochemistry in biopsies of patients with diabetic nephropathy. Data were analyzed using a Student’s t-test or a Mixed Model Regression Analysis. Double-labeled immunofluorescence was performed for endoglin and CD31 or VCAM-1. Differences were considered significant at p<0.05.


Lowering endoglin expression in endothelial cells in vitro significantly impaired VEGF-A- and glucose-mediated induction of activation markers VCAM1 and SELE, and significantly reduced monocyte adhesion (p<0.05). In diabetic patients, endoglin was primarily expressed in endothelial cells. Glomerular VCAM-1 expression co-localized with endoglin. Furthermore, glomerular VCAM-1 was significantly increased in patients with diabetic nephropathy (p<0.05) and correlated with glomerular endoglin levels (p<0.001).


Targeting endoglin function is a promising future strategy to interfere with endothelial activation in order to prevent or stop inflammation and thereby the progression of diabetic nephropathy.