title: 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.
authors.affiliation: Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.
authors.forename: Jaehoon
authors.initials: J
authors.lastname: Lee
authors.forename: Hye Jin
authors.initials: HJ
authors.lastname: Kim
authors.forename: Jung Ah
authors.initials: JA
authors.lastname: Moon
authors.forename: Young Hoon
authors.initials: YH
authors.lastname: Sung
authors.forename: In-Jeoung
authors.initials: IJ
authors.lastname: Baek
authors.forename: Jae-il
authors.initials: JI
authors.lastname: Roh
authors.forename: Na Young
authors.initials: NY
authors.lastname: Ha
authors.forename: Seung-Yeon
authors.initials: SY
authors.lastname: Kim
authors.forename: Young Yil
authors.initials: YY
authors.lastname: Bahk
authors.forename: Jong Eun
authors.initials: JE
authors.lastname: Lee
authors.forename: Tae Hyun
authors.initials: TH
authors.lastname: Yoo
authors.forename: Han-Woong
authors.initials: HW
authors.lastname: Lee
mesh_terms: D000818:Animals; D001189:Aryl Hydrocarbon Hydroxylases / Q000378:metabolism; D019363:Cytochrome P-450 CYP1A1 / Q000378:metabolism; D065633:Cytochrome P-450 CYP1B1; D004195:Disease Models, Animal; D005260:Female; D005786:Gene Expression Regulation / Q000502:physiology*; D006869:Hydronephrosis / Q000378:metabolism / Q000503:physiopathology*; D019746:Intramolecular Oxidoreductases / Q000235:genetics* / Q000502:physiology*; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D000071876:Prostaglandin-E Synthases; D018336:Receptors, Aryl Hydrocarbon / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology
chemical_list: D018336:Receptors, Aryl Hydrocarbon; D001189:Aryl Hydrocarbon Hydroxylases; C585496:CYP1B1 protein, human; C585498:Cyp1b1 protein, mouse; D019363:Cytochrome P-450 CYP1A1; D065633:Cytochrome P-450 CYP1B1; D019746:Intramolecular Oxidoreductases; D000071876:Prostaglandin-E Synthases