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Isolation and Culture of Cells from the Nephrogenic Zone of the Embryonic Mouse Kidney
08:06

Isolation and Culture of Cells from the Nephrogenic Zone of the Embryonic Mouse Kidney

Published on: April 22, 2011

Cell proliferation, apoptosis, Bcl-2 and Bax expression in obstructed opossum early metanephroi

H Liapis1, H Yu, G F Steinhardt

  • 1Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

The Journal of Urology
|July 14, 2000
PubMed
Abstract

Insights

Complete ureteral obstruction (CUTO) in fetal kidneys causes increased cell death and proliferation. Abnormal cell kinetics, including altered Bcl-2 and Bax gene expression, contribute to kidney disease pathogenesis.

Area of Science:

  • Developmental biology
  • Renal pathophysiology
  • Cellular and molecular mechanisms

Background:

  • Complete ureteral obstruction (CUTO) halts fetal kidney development, causing cysts and fibrosis.
  • Apoptosis is a known mechanism in chronically injured kidneys, but its role in fetal obstruction is unclear.

Purpose of the Study:

  • To investigate the roles of cell proliferation and apoptosis in fetal kidneys with CUTO.
  • To evaluate the expression of apoptosis-regulating genes, Bcl-2 and Bax, in obstructed fetal kidneys.

Main Methods:

  • Utilized opossum pups with early metanephric kidneys subjected to CUTO.
  • Kidneys were analyzed after two weeks for cell proliferation, apoptosis, and Bcl-2/Bax gene expression.

Main Results:

  • Obstructed kidneys showed increased apoptosis in the renal pelvis and tubulointerstitium compared to controls.
  • Apoptosis correlated with increased interstitial cell proliferation and altered Bcl-2/Bax expression in tubules.
  • The nephrogenic zone exhibited increased apoptosis and cell proliferation, with unchanged Bcl-2/Bax levels.

Conclusions:

  • Abnormal cell kinetics, including apoptosis and proliferation patterns, are implicated in the pathogenesis of obstructed fetal kidney disease.
  • Altered expression of apoptosis regulators like Bcl-2 and Bax may play a role in tubular injury.

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