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*Division of Nephrology, Department of Internal Medicine, University of Michigan, and Department of Veterans Affairs, Ann Arbor, Michigan; Institute for Anatomy and Cell Biology 1, University of Heidelberg, Heidelberg, Germany; and Institute for Anatomy, University of Zurich, Zurich, Switzerland.
Correspondence to Dr. Marcus J. Moeller, Institute for Anatomy and Cell Biology 1, University of Heidelberg, INF 307, 3.OG, D-69120 Heidelberg, Germany. Phone: +49-6221-548684; Fax: +49-6221-544951;
ABSTRACT. Cellular crescents are a defining histologic finding in many forms of inflammatory glomerulonephritis. Despite numerous studies, the origin of glomerular crescents remains unresolved. A genetic cell lineage-mapping study with a novel transgenic mouse model was performed to investigate whether visceral glomerular epithelial cells, termed podocytes, are precursors of cells that populate cellular crescents. The podocyte-specific 2.5P-Cre mouse line was crossed with the ROSA26 reporter line, resulting in irreversible constitutive expression of 
-galactosidase in doubly transgenic 2.5P-Cre/ROSA26 mice. In these mice, crescentic glomerulonephritis was induced with a previously described rabbit anti-glomerular basement membrane antiserum nephritis approach. Interestingly, -galactosidase-positive cells derived from podocytes adhered to the parietal basement membrane and populated glomerular crescents during the early phases of cellular crescent formation, accounting for at least one-fourth of the total cell mass. In cellular crescents, the proliferation marker Ki-67 was expressed in -galactosidase-positive and -galactosidase-negative cells, indicating that both cell types contributed to the formation of cellular crescents through proliferation in situ. Podocyte-specific antigens, including WT-1, synaptopodin, nephrin, and podocin, were not expressed by any cells in glomerular crescents, suggesting that podocytes underwent profound phenotypic changes in this nephritis model. E-mail: marcus.moeller@urz.uni-heidelberg.de
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