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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
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Published on: January 7, 2013

Simulated ischemia induces renal tubular cell apoptosis through a nuclear factor-kappaB dependent mechanism

K K Meldrum1, K Hile, D R Meldrum

  • 1Department of Urology, Johns Hopkins University, Baltimore, Maryland, USA.

The Journal of Urology
|June 7, 2002
PubMed
Abstract

Insights

Inhibition of nuclear factor-kappaB (NF-κB) prevents renal tubular cell apoptosis during ischemia-reperfusion injury. This study demonstrates NF-κB

Area of Science:

  • Nephrology
  • Cell Biology
  • Molecular Biology

Background:

  • Ischemia-reperfusion injury is a significant cause of acute renal failure.
  • Nuclear factor-kappaB (NF-κB) is implicated in the injury's pathophysiology.
  • The role of NF-κB inhibition in preventing renal tubular cell death is unclear.

Purpose of the Study:

  • To investigate the effect of NF-κB inhibition on ischemia-induced renal tubular cell death.
  • To determine if pyrrolidine dithiocarbamate (PDTC) can prevent apoptosis.

Main Methods:

  • Renal tubular cells (LLC-PK1) were subjected to simulated ischemia.
  • Cells were treated with or without PDTC, an NF-κB inhibitor.
  • NF-κB activation and apoptosis were assessed using electrophoretic mobility shift assay, immunohistochemistry, and TUNEL assay.

Main Results:

  • Simulated ischemia activated NF-κB and induced significant renal tubular cell apoptosis (62 +/- 5.2 apoptotic nuclei/hpf).
  • Pre-treatment with PDTC inhibited NF-κB activation.
  • PDTC treatment prevented ischemia-induced apoptosis (14 +/- 6 apoptotic nuclei/hpf).

Conclusions:

  • Simulated ischemia triggers NF-κB intranuclear translocation and activation in renal tubular cells.
  • NF-κB plays a mediating role in ischemia-induced renal tubular cell apoptosis.
  • Targeting NF-κB may offer therapeutic strategies for ischemic renal injury.

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