KAP Degradation by Calpain Is Associated with CK2 Phosphorylation and Provides a Novel Mechanism for Cyclosporine A-Induced Proximal Tubule Injury
2011

KAP Degradation by Calpain and Its Role in Cyclosporine A-Induced Kidney Injury

Sample size: 6 publication 10 minutes Evidence: high

Author Information

Author(s): Tornavaca Olga, Sarró Eduard, Pascual Gloria, Bardaji Beatriz, Montero M. Angeles, Salcedo M. Teresa, Plana Maria, López-Hellin Joan, Itarte Emilio, Meseguer Anna

Primary Institution: Institut de Recerca Vall d'Hebron, Hospital Universitari Vall d'Hebron, Barcelona, Spain

Hypothesis

Low KAP levels found in kidneys of CsA-treated mice might correlate with proximal tubule cell injury.

Conclusion

KAP protects proximal tubule cells from CsA-induced toxicity, suggesting a novel mechanism for CsA-induced kidney toxicity.

Supporting Evidence

  • KAP Tg mice showed no increase in kidney injury markers after CsA treatment.
  • CK2 inhibition protected against CsA-induced cytotoxicity.
  • KAP levels remained stable in CsA-treated Tg mice, unlike control littermates.

Takeaway

KAP is a protein that helps protect kidney cells, and when it's low due to a drug called cyclosporine A, the kidney cells can get hurt.

Methodology

The study used KAP transgenic mice and assessed the effects of cyclosporine A on kidney injury markers.

Participant Demographics

Male KAP-Tg mice and their littermates were used in the study.

Statistical Information

P-Value

p<0.0001

Statistical Significance

p<0.0001

Digital Object Identifier (DOI)

10.1371/journal.pone.0025746

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