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Journal of Biomedicine and Biotechnology
Volume 2011, Article ID 581928, 11 pages
Research Article

Approaching Biomarkers of Membranous Nephropathy from a Murine Model to Human Disease

1Division of Nephrology, Department of Medicine, Tri-Service General Hospital, Taipei 114, Taiwan
2Department of Microbiology and Immunology, National Defense Medical Center, Taipei 114, Taiwan
3Department of Pediatrics, Tri-Service General Hospital, Taipei 114, Taiwan
4Division of Nephrology, Department of Medicine, Cardinal Tien Hospital, Taipei 231, Taiwan
5Graduate Institute of Clinical Medicine, Taipei Medical University, 325, Cheng-Kung Road, Section 2, Nei-Hu, Taipei 114, Taiwan

Received 17 September 2010; Revised 2 December 2010; Accepted 10 December 2010

Academic Editor: Oreste Gualillo

Copyright © 2011 Chia-Chao Wu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Membranous glomerulonephropathy (MN) is the most prevalent cause of nephrotic syndrome in adult humans. However, the specific biomarkers of MN have not been fully elucidated. We examined the alterations in gene expression associated with the development of MN. Methods. Murine MN was induced by cationic bovine serum albumin (cBSA). After full-blown MN, cDNA microarray analysis was performed to identify gene expression changes, and highly expressed genes were evaluated as markers both in mice and human kidney samples. Results. MN mice revealed clinical proteinuria and the characteristic diffuse thickening of the glomerular basement membrane. There were 175 genes with significantly different expressions in the MN kidneys compared with the normal kidneys. Four genes, metallothionein-1 (Mt1), cathepsin D (CtsD), lymphocyte 6 antigen complex (Ly6), and laminin receptor-1 (Lamr1), were chosen and quantified. Mt1 was detected mainly in tubules, Lamr1 was highly expressed in glomeruli, and CtsD was detected both in tubules and glomeruli. The high expressions of Lamr1 and CtsD were also confirmed in human kidney biopsies. Conclusion. The murine MN model resembled the clinical and pathological features of human MN and may provide a tool for investigating MN. Applying cDNA microarray analysis may help to identify biomarkers for human MN.