Transgenic overexpression of p23 induces spontaneous hydronephrosis in mice.

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.

journal_name

Int J Exp Pathol

authors

Lee J,Kim HJ,Moon JA,Sung YH,Baek IJ,Roh JI,Ha NY,Kim SY,Bahk YY,Lee JE,Yoo TH,Lee HW

doi

10.1111/j.1365-2613.2011.00762.x

subject

Has Abstract

pub_date

2011-08-01 00:00:00

pages

251-9

issue

4

eissn

0959-9673

issn

1365-2613

journal_volume

92

pub_type

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