| First Author | Sorenson CM | Year | 1996 |
| Journal | Am J Physiol | Volume | 271 |
| Issue | 1 Pt 2 | Pages | F234-8 |
| PubMed ID | 8760267 | Mgi Jnum | J:34503 |
| Mgi Id | MGI:81959 | Doi | 10.1152/ajprenal.1996.271.1.F234 |
| Citation | Sorenson CM, et al. (1996) Abnormal renal development in the Os/+ mouse is intrinsic to the kidney. Am J Physiol 271(1 Pt 2):F234-8 |
| abstractText | 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. |
