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Abstract: TH-PO058

Overexpression of Preeclampsia Induced miR-26a-5p Leads to Proteinuria in Zebrafish

Session Information

Category: Glomerular

  • 1001 Glomerular: Basic/Experimental Immunology and Inflammation


  • Müller-Deile, Janina, Hannover medical school, Hanover, Germany
  • Schroder, Patricia Ann, Mount Desert Island Biological Laboratory, Salisbury Cove, Maine, United States
  • Nystrom, Jenny C., University of Gothenburg , Goteborg, Sweden
  • Haller, Hermann G., Hannover Medical School, Hannover, Germany
  • Schiffer, Mario, Hannover Medical School, Hannover, Germany

So far the pathomechanism of preeclampsia in pregnancy is focussed on increased circulating levels of sFLT1 that neutralizes glomerular VEGF-A expression and prevents its signalling at the glomerular endothelium. MiR-26a-5p is upregulated in the preeclamptic placenta.


We analyzed miR-26a-5p expression in podocytes and microinjected zebrafish eggs with a miR-26a-5p mimic. We analysed phenotype, proteinuria and ultrastructural changes of the glomerular filtration barrier.


We found that miR-26a-5p targets VEGF-A expression in cultured podocytes and that its overexpression in zebrafish causes proteinuria, edema, glomerular endotheliosis and podocyte foot process effacement. Recombinant zebrafish vegf-Aa protein could rescue glomerular changes induced by miR-26a-5p. Preeclamptic patients with podocyte damage identified by podocyturia, expressed significantly more urinary miR-26a-5p compared to controls.


Thus, functional and ultrastructural glomerular changes after miR-26a-5p overexpression can resemble the findings seen in preeclampsia and indicate a potential pathophysiological role of miR-26a-5p in addition to sFLT-1 in this disease.