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The contribution of glomerular endothelial cells to hyperglycemia-induced glo-merular basement membrane thickening, and its effect on modified hyaluronan metabo-lism, inflammation and fibrosis during the development of diabetic nephropathy

Supervisor (Mannheim): Jonathan Sleeman
Co-Supervisor (Groningen): Jacob van den Born
Graduate: Michael Albrecht

Project description

In this project we will investigate three major questions: (i) Which extracellular matrix (ECM) components produced by glomerular endothelial cells (gEC) in response to hyperglycemia contribute to the thickening of the glomerular basement membrane (GBM)? (ii) How does the response of podocytes to the modified content and conformation of the thickened GBM contribute to inflammation, fibrosis and modified hyaluronic acid (HA) metabolism in the nephrotic kidney? (iii) How does modified HA metabolism contribute to diabetic nephropathy?


  1. *Fieber et al J Cell Sci 2004;117:359-67
  2. *Schmaus et al Brit J Cancer 2014;111:559-67
  3. *Schmaus et al Glycobiology 2015;25:258-68
  4. *Schmaus et al Cancer Metastasis Rev 2014;33:1059-79
  5. Byron et al J Am Soc Nephrol 2014;25:1-14
  6. Ikegami-Kawai et al J Biochem 2003;134,875–80
  7. Kanasaki et al Frontiers Endocrinol 2013;4:1-15
  8. Savige J Physiol 2014; 592.18:4013–23
  9. Stridh et al AJP-RICP 2012;302:R1235–R1249

* Own publications

Methods used

Cultivation of human gEC and podocytes, MALDI-TOF MS, RNAseq, qPCR, analysis of STZ-induced mouse model of diabetes and genetically modified mice, isolation of interstitial fluid.

Collaboration Partners

  • Jacob van den Born, Groningen
  • Peter Nawroth, Heidelberg
  • Jens Kroll, Mannheim
  • Benito Yard, Mannheim