• nephrogenesis;
  • apoptosis;
  • nephron numbers


Bcl-2 is the founding member of a family of proteins that influence apoptosis. Loss of bcl-2 results in renal hypoplasia/cystic dysplasia at birth. Here, we examined whether re-expression of bcl-2 throughout the ureteric bud and its derived epithelia would restore a normal renal phenotype in bcl-2 −/− mice. Re-expression of bcl-2 in the ureteric bud/collecting duct of bcl-2 −/− mice increased nephron numbers, diminished glomerular hypertrophy, and increased nephrogenic zone size. Unlike bcl-2 −/− mice which have gross renal cyst formation, few renal cysts were present in mice re-expressing bcl-2. We have previously shown increased apoptosis and proliferation, as well as aberrant protein tyrosine phosphatase 1B expression, accompanied cystic changes in bcl-2 −/− mice. These changes were not observed when bcl-2 was re-expressed in the ureteric bud/collecting duct system. Thus, expression of bcl-2 in the ureteric bud/collecting duct resulted in increased nephron numbers partially rescuing renal hypoplasia/cystic dysplasia in bcl-2 −/− mice. Developmental Dynamics 237:2450–2459, 2008. © 2008 Wiley-Liss, Inc.