AJP - Renal Physiology, Vol 271, Issue 1 234-F238, Copyright © 1996 by American Physiological Society
Abnormal renal development in the Os/+ mouse is intrinsic to the kidney
C. M. Sorenson, S. A. Rogers and M. R. Hammerman
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.
