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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Published on: January 7, 2013

PAX2 suppresses apoptosis in renal collecting duct cells

E Torban1, M R Eccles, J Favor

  • 1Department of Pediatrics and Experimental Medicine, McGill University, Montreal, Quebec, Canada.

The American Journal of Pathology
|September 12, 2000
PubMed

Insights

The transcription factor PAX2 (paired box gene 2) is crucial for kidney development. Reduced PAX2 levels increase ureteric bud cell death, leading to renal hypoplasia and fewer nephrons.

Area of Science:

  • Developmental Biology
  • Genetics
  • Cell Biology

Background:

  • PAX2 (paired box gene 2) is a key transcription factor in central nervous system and genitourinary axis development.
  • Mutations in PAX2 cause renal-coloboma syndrome, featuring optic nerve colobomas and renal hypoplasia.
  • PAX2 mutant mice exhibit reduced ureteric bud branching and nephron formation, linked to increased apoptosis.

Purpose of the Study:

  • To investigate the direct role of PAX2 in regulating ureteric bud (UB) cell survival during nephrogenesis.
  • To determine if apoptosis is directly correlated with PAX2 expression levels in renal cells.

Main Methods:

  • Studied PAX2's role in cultured renal cells, including mIMCD-3 (murine collecting duct) and HEK293 cells.
  • Utilized anti-sense PAX2 transfection in mIMCD-3 cells to assess apoptosis.
  • Investigated the effect of exogenous PAX2 expression in HEK293 cells on caspase-2-induced apoptosis.
  • Assessed PAX2's impact on proliferation in embryonic kidney and cultured kidney cells.

Main Results:

  • High endogenous PAX2 expression in mIMCD-3 cells correlated with resistance to apoptosis; anti-sense PAX2 transfection induced apoptosis.
  • Exogenous PAX2 expression in HEK293 cells conferred protection against caspase-2-induced apoptosis.
  • PAX2 did not influence the proliferation of embryonic kidney or cultured kidney cells.

Conclusions:

  • PAX2 plays a direct role in promoting the survival of ureteric bud cells during kidney development.
  • This finding clarifies the mechanism underlying renal hypoplasia in PAX2-related disorders.
  • PAX2 is essential for preventing excessive apoptosis in developing renal structures.

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