足细胞
突触素
尼福林
肾小球基底膜
肾小球肾炎
肾炎
波多辛
细胞标志蛋白
基底膜
生物
细胞生物学
转基因小鼠
病理
转基因
免疫学
分子生物学
肾
内分泌学
医学
蛋白尿
生物化学
基因
作者
Marcus J. Moeller,Abdulsalaam Soofi,Inge Hartmann,Michel Le Hir,Roger C. Wiggins,Wilhelm Kriz,Lawrence B. Holzman
出处
期刊:Journal of The American Society of Nephrology
日期:2004-01-01
卷期号:15 (1): 61-67
被引量:175
标识
DOI:10.1097/01.asn.0000102468.37809.c6
摘要
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 β-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, β-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 β-galactosidase-positive and β-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: [email protected]
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