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Abnormal postpartum renal development and cystogenesis in the bcl-2 (-/-) mouse
C M Sorenson1, B J Padanilam, M R Hammerman
1George M. O'Brien Kidney and Urological Diseases Center, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
The American Journal of Physiology
|July 1, 1996
Summary
Mice lacking B cell leukemia/lymphoma gene 2 (bcl-2) develop kidney cysts due to abnormal cell growth and death during development. This research clarifies the role of bcl-2 in kidney cyst formation.
Area of Science:
- Nephrology
- Developmental Biology
- Molecular Biology
Background:
- Mice lacking B cell leukemia/lymphoma gene 2 (bcl-2) exhibit congenital renal hypoplasia and develop multicystic kidney disease and renal failure postnatally.
- Understanding the cellular mechanisms underlying bcl-2 deficiency-induced kidney disease is crucial for identifying therapeutic targets.
Purpose of the Study:
- To characterize postpartum kidney development in bcl-2 deficient mice.
- To identify the cellular origin of cysts in bcl-2 deficient kidneys.
- To elucidate the role of bcl-2 deficiency in the cystogenic process.
Main Methods:
- Comparative morphological examination of kidneys from bcl-2 knockout and wild-type mice from birth to P28.
- Assessment of cellular proliferation (using 5-bromo-2'-deoxyuridine incorporation) and apoptosis.
- Characterization of bcl-2-related protein, bax, expression.
Main Results:
- Kidneys from bcl-2 (-/-) mice showed reduced weight gain and cyst development in proximal tubules, distal tubules, and collecting ducts post-P7.
- Compensatory growth was observed in unaffected glomeruli and proximal tubules.
- Cystogenesis was associated with enhanced proliferation and apoptosis, with bax protein expressed in some cysts.
Conclusions:
- Abnormal regulation of DNA synthesis and apoptosis accompanies cystogenesis in bcl-2 deficient mice during postpartum kidney development.
- Continued bax expression may contribute to enhanced apoptotic cell death in the developing kidneys.