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Transgenic overexpression of p23 induces spontaneous hydronephrosis in mice

Title
Transgenic overexpression of p23 induces spontaneous hydronephrosis in mice
Authors
Jaehoon Lee;Hye Jin Kim;Han-Woong Lee;Tae Hyun Yoo;Jong Eun Lee;Young Yil Bahk;Seung-Yeon Kim;Na Young Ha;Jae-il Roh;In-Jeoung Baek;Young Hoon Sung;Jung Ah Moon
Issue Date
2011
Journal Title
International Journal of Experimental Pathology
ISSN
0959-9673
Citation
International Journal of Experimental Pathology, Vol.92(4) : 251~259, 2011
Abstract
p23 is a cochaperone of heat shock protein 90 and also interacts functionally with numerous steroid receptors and kinases. However, the in vivo roles of p23 remain unclear. To explore its in vivo function, we generated the transgenic (TG) mice ubiquitously overexpressing p23. The p23 TG mice spontaneously developed kidney abnormalities closely resembling human hydronephrosis. Consistently, kidney functions deteriorate significantly in the p23 TG mice compared to their wild-type (WT) littermates. Furthermore, the expression of target genes for aryl hydrocarbon receptor (AhR), such as cytochrome P450, family 1, subfamily A, polypeptide 1 (Cyp1A1) and cytochrome P450, family 1, subfamily B, polypeptide 1 (Cyp1B1), were induced in the kidneys of the p23 TG mice. These results indicate that the overexpression of p23 contributes to the development of hydronephrosis through the upregulation of the AhR pathway in vivo.
URI

http://ir.ymlib.yonsei.ac.kr/handle/22282913/94002
DOI
10.1111/j.1365-2613.2011.00762.x
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Internal Medicine
1. 연구논문 > 1. College of Medicine > Dept. of Anatomy
Yonsei Authors
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