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Effects of Specific Genes Activating RAGE on Polycystic Kidney Disease

Authors
Park, Eun YoungSeo, Min JiPark, Jong Hoon
Issue Date
Aug-2010
Publisher
KARGER
Keywords
Autosomal-dominant polycystic kidney disease; Receptor of advanced glycation end product; Cell proliferation; Cystogenesis
Citation
AMERICAN JOURNAL OF NEPHROLOGY, v.32, no.2, pp.169 - 178
Journal Title
AMERICAN JOURNAL OF NEPHROLOGY
Volume
32
Number
2
Start Page
169
End Page
178
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13595
DOI
10.1159/000315859
ISSN
0250-8095
Abstract
Background: Autosomal-dominant polycystic kidney disease (ADPKD) is characterized by progressive cyst formation and secretion of fluid and is associated with interstitial inflammation and fibrosis, resulting in the loss of renal function. We previously generated mice overexpressing PKD2, causing progressive cyst development with an inflammatory and fibrotic phenotype in the kidneys. Methods: To profile the gene expression related to inflammation and cystogenesis, microarray analysis was performed with kidney tissue from 6-, 12- and 18-month-old mice. Subsequently, levels and related mechanisms of selected genes, s100a8 and s100a9, were evaluated. Results: S100a8 and s100a9 was upregulated more than 2-fold and differently expressed in the cystic region. Receptor of advanced glycation end product (RAGE) is a putative cell surface receptor for s100a8/a9. It was expressed in cyst-lining cells and up-regulated pro-inflammatory transcription factor NF-kappa B in transgenic mice. We also confirmed RAGE expression in ADPKD patient kidneys. It was suggested that the signaling related to proliferative cystogenesis through previous reports; therefore, we confirmed that phosphorylated-ERK and cyst formation was reduced by treatment of RAGE-siRNA. Conclusions: The results may provide important information for the expression of s100a8/a9 and RAGE, linking progressive cystogenesis with inflammation in cystic kidney. Copyright (C) 2010 S. Karger AG, Basel
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