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Am J Physiol. 1996 Jul;271(1 Pt 2):F234-8.

Abnormal renal development in the Os/+ mouse is intrinsic to the kidney.

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George M. O'Brien Kidney and Urological Diseases Center, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.


The oligosyndactylism (Os/+) mouse, is a genetic model for oligomeganephronic congenital renal hypoplasia. To define the abnormality in renal development and to determine whether the abnormality is kidney autonomous, we examined kidneys from newborn and 21- and 63-day-old Os/+ and wild-type (+/+) mice, obtained metanephric kidneys from embryonic day 12 (E12) Os/+ and +/+ embryos, and compared growth and development of the metanephroi in vitro. Kidneys from newborn Os/+ mice were smaller than those from newborn +/+ mice and contained fewer glomeruli per midsagittal section. Following birth, kidneys from Os/+ mice manifest compensatory growth of glomeruli and proximal tubules. Metanephroi from E12 Os/+ and +/+ embryos were comparable in size. However, during 4 days in culture, growth and development of metanephroi from Os/+ embryos were visibly reduced compared with metanephroi from +/+ embryos. Expression of B cell leukemia/lymphoma gene 2 (bcl-2), the absence of which is known to result in congenital renal hypoplasia, was detected in the Os/+ mouse kidneys. We conclude that the renal abnormality in Os/+ mice is intrinsic to the kidney and does not result from the absence of bcl-2 expression.

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