Nuclear localization of β-catenin and loss of apical brush border actin in cystic tubules of bcl-2 −/− mice

• Published in: American journal of physiology. Renal physiology 1999-02, Vol.276 (2), p.F210-F217
• Main Author: Sorenson, Christine M.
• Format: Article
• Language: English
• ISSN: 1931-857X; 1522-1466
• DOI: 10.1152/ajprenal.1999.276.2.F210

Tight regulation of the rates of cell proliferation and apoptosis is critical for normal nephrogenesis. Nephrogenesis is profoundly affected by the loss of bcl-2 expression. Bcl-2-deficient (bcl-2 −/−) mice are born with renal hypoplasia and succumb to renal failure secondary to renal multicystic disease. Cell-cell and cell-matrix interactions impact tissue architecture by modulating cell proliferation, migration, differentiation, and apoptosis. E-cadherin mediates calcium-dependent homotypic cell-cell interactions that are stabilized by its association with catenins and the actin cytoskeleton. The contribution of altered cell-cell interactions to renal cystic disease has not been delineated. Cystic kidneys from bcl-2 −/− mice displayed nuclear localization of β-catenin and loss of apical brush border actin staining. The protein levels of α-catenin, β-catenin, actin, and E-cadherin were not altered in cystic kidneys compared with normal kidneys. Therefore, an altered distribution of β-catenin and actin, in kidneys from bcl-2 −/− mice, may indicate improper cell-cell interactions interfering with renal maturation and contributing to renal cyst formation.