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Genetics and Development |



* Center for Cell and Developmental Biology, Columbus Childrens Research Institute and
Department of Radiology, Columbus Childrens Hospital and
Division of Sensory Biophysics, The Ohio State University, Columbus, and
Zoology Department, Miami University, Oxford, Ohio
Address correspondence to: Dr. Kirk M. McHugh, Columbus Childrens Research Institute, 700 Childrens Drive, Suite WA 2014, Columbus, OH 43205. Phone: 614-355-2817; Fax: 614-722-5892; mchughk{at}ccri.net
Received for publication April 27, 2006. Accepted for publication November 7, 2006.
Urinary tract malformations, obstructive uropathy, and hypoplasia/dysplasia are extremely important in terms of pediatric health care costs, with end-stage renal failure in children estimated to cost >$15 billion annually in the United States alone. Even so, little is known regarding the mechanisms that control these processes. Identified was a unique mutant mouse model that develops in utero megabladder, resulting in variable hydroureteronephrosis and chronic renal failure secondary to obstructive uropathy. These animals, designated mgb for megabladder, possess a primary defect in bladder smooth muscle development that is apparent by embryonic day 15. The mgb mouse represents an excellent model for the study of normal and pathogenic bladder development, including the postnatal progression of chronic renal failure that results from the development of in utero obstructive uropathy.
Related Article
J. Am. Soc. Nephrol. 2007 18: 353-355.
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