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Recruitment of Podocytes from Glomerular Parietal Epithelial Cells

Daniel Appel^*, David B. Kershaw, Bart Smeets^*,, Gang Yuan^*, Astrid Fuss^*, Björn Frye^*, Marlies Elger, Wilhelm Kriz, Jürgen Floege^* and Marcus J. Moeller^*

^* Division of Nephrology and Immunology, Rheinisch Westfälische Technische Hochschule (RWTH) University of Aachen, Aachen, Germany; Division of Nephrology, Department of Pediatrics, University of Michigan, Ann Arbor, Michigan; Department of Pathology, Radboud University Nijmegen Medical Center, Nijmegen, Netherlands; and Institute for Anatomy and Cell Biology, University of Heidelberg/Mannheim, Mannheim, Germany

Correspondence: Dr. Marcus J. Moeller, Department of Nephrology and Clinical Immunology, RWTH University Hospital Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany. Phone: ++49-241-8089530; Fax: ++49-241-8082446; E-mail: mmoeller{at}ukaachen.de

Received for publication July 29, 2008. Accepted for publication October 5, 2008.

Loss of a critical number of podocytes from the glomerular tuft leads to glomerulosclerosis. Even in health, some podocytes are lost into the urine. Because podocytes themselves cannot regenerate, we postulated that glomerular parietal epithelial cells (PECs), which proliferate throughout life and adjoin podocytes, may migrate to the glomerular tuft and differentiate into podocytes. Here, we describe transitional cells at the glomerular vascular stalk that exhibit features of both PECs and podocytes. Metabolic labeling in juvenile rats suggested that PECs migrate to become podocytes. To prove this, we generated triple-transgenic mice that allowed specific and irreversible labeling of PECs upon administration of doxycycline. PECs were followed in juvenile mice beginning from either postnatal day 5 or after nephrogenesis had ceased at postnatal day 10. In both cases, the number of genetically labeled cells increased over time. All genetically labeled cells coexpressed podocyte marker proteins. In conclusion, we demonstrate for the first time recruitment of podocytes from PECs in juvenile mice. Unraveling the mechanisms of PEC recruitment onto the glomerular tuft may lead to novel therapeutic approaches to renal injury.

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