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Originally published In Press as doi:10.1074/jbc.M102916200 on April 25, 2001

J. Biol. Chem., Vol. 276, Issue 31, 29410-29419, August 3, 2001
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Kidney Androgen-regulated Protein Interacts with Cyclophilin B and Reduces Cyclosporine A-mediated Toxicity in Proximal Tubule Cells*

Cristina CebriánDagger , Cristina ArestéDagger , Antoni NicolásDagger , Pere OlivéDagger , Ana Carceller§, Jaume Piulats§, and Anna MeseguerDagger

From the Dagger  Centre d'Investigacions en Bioquímica i Biologia Molecular, Hospital Universitari Vall d'Hebron, Pg. Vall d'Hebron 119-129, Plta. 14, 08035 Barcelona, Spain and the § Laboratorio de Bioinvestigación, Merck Farma y Química, S.A., 08010 Barcelona, Spain

The gene for kidney androgen-regulated protein (KAP) is the most abundant and specific gene expressed in mouse kidney proximal tubule cells, where it is tightly regulated by steroid and thyroid hormones in different tubule segments. Despite the cell-specific expression, strict regulatory mechanisms, and relative abundance, nothing is known of the function of its encoded protein, which does not exhibit known structural or functional domains, or homologies with other sequences in the data bases. We raised monoclonal antibodies against KAP, which specifically recognize a protein with an apparent molecular mass of 20 kDa in crude kidney homogenates, the distribution and regulation of which parallel that of its mRNA. To gain insight into its function, we performed a yeast two hybrid screen and determined that KAP specifically interacts with cyclophilin B. Furthermore, cyclosporine A (CsA)-treated mice exhibited a significant decrease in KAP levels, and tetracycline-controlled overexpression of KAP in stably transfected proximal tubule cells significantly decreased the toxic effects of CsA. Taken together, these results indicate a functional relationship among KAP-, cyclophilin B-, and CsA-mediated nephrotoxicity and suggest an important role of KAP in renal physiology, providing new data on the molecular mechanisms implied in the toxic effects of CsA.

* This work was supported by Grant PM97-0095 from the Ministerio de Educacion y Cultura, Programa Sectorial de Promoción General del Conocimiento. This work has been awarded the Iñigo Alvarez de Toledo prize for the basic research in Nephrology (Edition XII, 2000).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed. Tel.: 34-93-4894061; Fax: 34-93-4894064; E-mail: meseguer@hg.vhebron.es.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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