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*Division of Nephrology and Immunology and
Interdisciplinary Centre for Clinical Research "BIOMAT", University Hospital of the Aachen University of Technology, Aachen, Germany; and
Departments of
Pathology and
Nephrology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands
Correspondence: Dr. Marcus J. Moeller, Department of Nephrology and Immunology, University Hospital of the Aachen University of Technology, Pauwelsstrasse 30, 52074 Aachen, Germany. Phone: ++49-241-8089530; Fax: ++49-241-8082446; E-mail: mmoeller{at}ukaachen.de
Received for publication January 30, 2009. Accepted for publication September 22, 2009.
Cellular lesions form in Bowman's space in both crescentic glomerulonephritis and collapsing glomerulopathy. The pathomechanism and origin of the proliferating cells in these lesions are unknown. In this study, we examined proliferating cells by lineage tracing of either podocytes or parietal epithelial cells (PECs) in the nephrotoxic nephritis model of inflammatory crescentic glomerulonephritis. In addition, we traced the fate of genetically labeled PECs in the Thy-1.1 transgenic mouse model of collapsing glomerulopathy. In both models, cellular bridges composed of PECs were observed between Bowman's capsule and the glomerular tuft. Genetically labeled PECs also populated larger, more advanced cellular lesions. In these lesions, we detected de novo expression of CD44 in activated PECs. In contrast, we rarely identified genetically labeled podocytes within the cellular lesions of crescentic glomerulonephritis. In conclusion, PECs constitute the majority of cells that compose early extracapillary proliferative lesions in both crescentic glomerulonephritis and collapsing glomerulopathy, suggesting similar pathomechanisms in both diseases.
Related Article
J. Am. Soc. Nephrol. 2009 20: A10.
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