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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

Calpains mediate acute renal cell death: role of autolysis and translocation

X Liu1, J J Rainey, J F Harriman

  • 1Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

American Journal of Physiology. Renal Physiology
|September 13, 2001
PubMed

Insights

Calpains contribute to kidney proximal tubule injury by leaking from cells after damage. A calpain inhibitor, PD-150606, prevents cell death and aids functional recovery in injured renal proximal tubules.

Area of Science:

  • Nephrology
  • Cell Biology
  • Biochemistry

Background:

  • Calpains are calcium-dependent proteases implicated in various cellular processes.
  • Their role in renal proximal tubule (RPT) injury is not fully understood.
  • Understanding calpain activity is crucial for developing therapeutic strategies for kidney injury.

Purpose of the Study:

  • To investigate the expression and behavior of calpain isoforms in rabbit RPT.
  • To examine calpain autolysis and translocation during RPT injury.
  • To evaluate the protective effects of a calpain inhibitor (PD-150606) on RPT function.

Main Methods:

  • RT-PCR and immunoblot analysis for calpain isoform expression.
  • FITC-casein zymography to assess protease activity.
  • Mitochondrial inhibitor (antimycin A) and hypoxia/reoxygenation models for RPT injury.
  • Assessment of cell death, membrane permeability, mitochondrial function, and ion transport.

Main Results:

  • Rabbit RPT express only mu- and m-calpains.
  • Mitochondrial inhibition led to cell death and increased permeability but not calpain autolysis or translocation.
  • PD-150606 inhibited cell death, preserved calpain levels, and restored mitochondrial function and Na+ transport after injury.
  • Calpains appear to leak from damaged RPT rather than translocate or autolyze within the cell.

Conclusions:

  • Calpains mediate RPT injury through a mechanism not involving autolysis or translocation.
  • Calpains are released from RPT following injury and cell death.
  • PD-150606 demonstrates therapeutic potential by protecting RPT and promoting functional recovery post-injury.

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