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Kidney Week

Abstract: FR-PO925

Injured Podocytes Show an Increased Responsiveness to Angiotensin II-Mediated Calcium Transients

Session Information

Category: Glomerular Diseases

  • 1204 Podocyte Biology


  • Binz, Julia, University Hospital Cologne, Cologne, Germany
  • Ester, Lioba, University Hospital Cologne, Cologne, Germany
  • Schermer, Bernhard, University Hospital Cologne, Cologne, Germany
  • Benzing, Thomas, University Hospital Cologne, Cologne, Germany
  • Hackl, Matthias, University Hospital Cologne, Cologne, Germany

Angiotensin II (AngII) signaling has been shown to play a role in regulating glomerular perfusion and progression in kidney disease. The treatment of patients with ACE inhibitors is well established. Furthermore, AngII has shown to be able to trigger calcium signals podocytes ex vivo. In this study we aimed at unravelling AngII induced calcium signaling in healthy and diseased podocytes in vivo.


Kidney disease was induced in 4 week old mice expressing the calcium indicator GCaMP3 in podocytes (Pod:cre) by injecting 25 mg/kg Adriamycin. 4 days after injection the mice underwent 2-photon in vivo imaging. Mice were anaesthetized, a vascular access generated and the left kidney exteriorized. The vasculature was labelled with a 70 kDa dextrane (Texas Red). Untreated GCaMP3 Pod:cre animals were used as controls. AngII was infused with 100 ng/g/min. As inhibitors Losartan (10 mg/kg) and PD123319 (10 mg/kg) were used. The induced calcium transients were recorded as time lapse videos with 1 frame/second. The percentage of podocyte area showing an increase in calcium levels was calculated using ImageJ.


The data shows that in 21 % of healthy glomeruli and in a mean of 2 podocytes a calcium signal can be triggered by AngII. The probability of inducing a calcium transient in a glomerulus by AngII stimulation increased by two-fold (41 %) in diseased (ADR) podocytes. Furthermore, the number of podocytes showing calcium transients is significantly increased. These findings correlate with a rise in the percentage of podocyte area showing a calcium signal from 12 to 26 %. The AngII induced calcium transient can be completely blocked by using Losartan, but not by PD123319.


Our study shows that calcium signaling in podocytes is highly regulated and the response to AngII increases upon injury. Additionally, we observed that not all podocytes react to AngII which points to heterogeneity in the podocyte population during health and disease. We can show that AngII mediates its calcium effects through the AT1R since Losartan completely blocked the calcium signal in podoyctes. Therefore our results strongly support the need of a RAAS blockade in glomerular disease to protect podocytes from high calcium levels induced by AngII.