Preeclamptic sera directly induce slit-diaphragm protein redistribution and alter podocyte barrier-forming capacity.

Background/aims: Podocytes are critical in maintaining the filtration barrier of the glomerulus and are dependent on the slit diaphragm. We hypothesized that disturbances of podocyte biology contribute to proteinuria in women with preeclampsia (PE).
Methods: A human podocyte cell line was stimulated with serum from women with PE (patients) and healthy pregnant women (controls); the main changes in 3 important podocyte proteins: podocin, CD2AP and actin were established by immunofluorescence and Western blot; we also searched for changes in cell plasticity by measuring the resistance of cultured podocytes.
Results: Different distributions of CD2AP, podocin and actin were observed in the podocytes stimulated with patient sera compared to podocytes stimulated with control sera. We also found that the mean resistance value of podocytes cultured with serum from women with PE was significantly lower than podocytes cultured with serum from controls. There was no difference in the protein expression level of podocin and CD2AP between patients and controls.
Conclusions: We present evidence that there are differences in podocytes when stimulated with sera from women with PE compared to those stimulated with healthy pregnancy sera. This is the first time that podocyte alterations have been directly related to PE; these descriptive findings could be considered as an interesting beginning for further studies relating podocytes and PE.
(Copyright 2008 S. Karger AG, Basel.)