Abnormal renal development in the os/+mouse is intrinsic to the
kidney.
Sorenson, Christine M., Sharon A. Rogers, and Marc R. Hammerman.
George M. O'Brien Kidney and Urological Diseases Center,
Departments of Medicine and Cell Biology and Physiology, Washington
University School of Medicine, St. Louis, Missouri, 63110
APStracts 3:0080F, 1996.
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,
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 mid-sagittal 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 to 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.
Received 15 February 1996; accepted in final form 5 April 1996.
APS Manuscript Number F52-6.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 May 96