Approaching biomarkers of membranous nephropathy from a murine model to human disease

Yuh Feng Lin, Chia Chao Wu, Jin Shuen Chen, Ching Feng Huang, Chun Chi Chen, Kuo Chen Lu, Pauling Chu, Huey Kang Sytwu

研究成果: 雜誌貢獻文章同行評審

20 引文 斯高帕斯(Scopus)

摘要

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.

原文英語
文章編號581928
期刊Journal of Biomedicine and Biotechnology
2011
DOIs
出版狀態已發佈 - 2011

ASJC Scopus subject areas

  • 生物技術
  • 分子醫學
  • 遺傳學
  • 分子生物學
  • 健康、毒理學和誘變
  • 醫藥 (全部)

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