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Rescue of renal hypoplasia and cystic dysplasia in Bcl‐2 −/− mice expressing Bcl‐2 in ureteric bud derived epithelia
Author(s) -
Kondo Shuji,
Oakes Mason G.,
Sorenson Christine M.
Publication year - 2008
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.21678
Subject(s) - ureteric bud , biology , nephron , hypoplasia , renal dysplasia , kidney , dysplasia , kidney development , endocrinology , cyst , mesonephric duct , medicine , pathology , anatomy , embryonic stem cell , genetics , gene , biochemistry
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.