Tracing the Origin of Glomerular Extracapillary Lesions from Parietal Epithelial Cells

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 e...

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Bibliographic Details
Published in:Journal of the American Society of Nephrology 2009-12, Vol.20 (12), p.2604-2615
Main Authors: SMEETS, Bart, UHLIG, Sandra, FUSS, Astrid, MOOREN, Fieke, WETZELS, Jack F. M, FLOEGE, Jürgen, MOELLER, Marcus J
Format: Article
Language:English
Subjects:
Animals
Basic Research
Biological and medical sciences
Bowman Capsule - metabolism
Bowman Capsule - pathology
Cell Proliferation
Claudin-1
Disease Models, Animal
Epithelial Cells - metabolism
Epithelial Cells - pathology
Glomerulonephritis - metabolism
Glomerulonephritis - pathology
Hyaluronan Receptors - metabolism
Hyperplasia
Kidney Glomerulus - metabolism
Kidney Glomerulus - pathology
Medical sciences
Membrane Proteins - metabolism
Mice
Mice, Transgenic
Nephrology. Urinary tract diseases
Podocytes - metabolism
Podocytes - pathology
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Summary: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.
ISSN:1046-6673
1533-3450
DOI:10.1681/asn.2009010122