Kid-1 expression is high in differentiated renal proximal tubule cells and suppressed in cystic epithelia. Witzgall, Ralph, Nicholas Oberm[umlaut]uller, Ulrike B[diaeresis]olitz, James P. Calvet, Benjamin D. Cowley, Jr., Cheryl Walker, Wilhelm Kriz, Norbert Gretz, Joseph V. Bonventre. 1Institute of Anatomy and Cell Biology I, University of Heidelberg, 69120 Heidelberg, Germany; 2Medical Research Center, Klinikum Mannheim, University of Heidelberg, Mannheim, Germany; 3Kansas University Medical Center, Kansas, U.S.A.; 4University of Texas M. D. Anderson Cancer Center, Smithville, TX 78957; 5Renal Unit and Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, U.S.A.
APStracts 5:0157F, 1998.
The cDNA coding for the transcriptional repressor protein Kid-1 was cloned in a screen for zinc finger proteins which are regulated during renal development and after renal ischemia. Kid-1 mRNA levels increase in the course of postnatal renal development and decrease after acute renal injury caused by ischemia or administration of folic acid. We have raised a monoclonal anti-Kid-1 antibody and demonstrate that the Kid-1 protein is strongly expressed in the proximal tubule of the adult rat kidney. During nephron development, the Kid-1 protein appears after the S-shaped body stage concomitantly with the brush border enzyme alkaline phosphatase. In two animal models of polycystic kidney disease, the expression of Kid-1 is downregulated. The loss of expression of Kid-1 in cyst wall cells correlates with the loss of alkaline phosphatase histochemical staining. Kid-1 mRNA levels are also reduced in rodent renal cell carcinomas, another condition characterized by epithelial cell dedifferentiation and increased proliferation. We propose that Kid-1 may play an important role during the differentiation of the proximal tubule.

Received 13 March 1998; accepted in final form 3 September 1998.
APS Manuscript Number F65-8.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 21 September 1998