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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
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Calpain 10 is required for cell viability and is decreased in the aging kidney

Marisa D Covington1, David D Arrington, Rick G Schnellmann

  • 1Department of Pharmaceutical and Biomedical Sciences, Center for Cell Death, Injury, and Regeneration, South Carolina College of Pharmacy, Medical University of South Carolina, Charleston, South Carolina 29425, USA.

American Journal of Physiology. Renal Physiology
|January 16, 2009
PubMed

Insights

Mitochondrial calpain 10 (an enzyme) is crucial for kidney cell survival. Its levels decline with age in rat, mouse, and human kidneys, indicating its role in aging kidney function.

Area of Science:

  • Biochemistry
  • Gerontology
  • Nephrology

Background:

  • Aging is linked to kidney dysfunction, but underlying mechanisms remain unclear.
  • Calpains are calcium-dependent proteases implicated in cellular processes.

Purpose of the Study:

  • To investigate the role of calpains 1, 2, and 10 in kidney aging.
  • To determine if calpain 10 is essential for kidney cell viability.

Main Methods:

  • Assessed calpain protein and mRNA levels in aging rat, mouse, and human kidney tissues.
  • Utilized shRNA to reduce calpain 10 in rabbit renal proximal tubular cells (RPTC).
  • Examined markers of apoptosis following calpain 10 knockdown.

Main Results:

  • Calpain 10 protein levels decreased in aging rat, mouse, and human kidneys, but not livers.
  • Caloric restriction attenuated the age-related decline in rat kidney calpain 10.
  • Mitochondrial calpain 10 depletion induced apoptosis in RPTC.

Conclusions:

  • Mitochondrial calpain 10 is essential for renal cell viability.
  • Decreased calpain 10 in aging kidneys correlates with declining renal function.
  • Calpain 10 may serve as a biomarker for kidney aging.

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