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Related Experiment Videos

Postischemic function and protein kinase C signal transduction

T J Rohs1, K S Kilgore, A J Georges

  • 1Section of Thoracic Surgery, University of Michigan Medical Center, Ann Arbor, USA.

The Annals of Thoracic Surgery
|July 1, 1998
PubMed
Summary

Pharmacologic induction of protein kinase C (PKC) translocation improves heart function after ischemia. This protective effect is not due to changes in metabolism, suggesting PKC translocation as a therapeutic target.

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[Ischemic preconditioning of the heart can be simulated by pharmacologic hibernation enkephalins].

Langenbecks Archiv fur Chirurgie. Supplement. Kongressband. Deutsche Gesellschaft fur Chirurgie. Kongress·2003

Area of Science:

  • Cardiovascular Science
  • Molecular Biology
  • Biochemistry

Background:

  • Myocardial preconditioning offers protection against ischemia through various mechanisms.
  • G-protein-mediated protein kinase C (PKC) translocation is a key pathway in this protective effect.

Purpose of the Study:

  • To investigate the pharmacologic induction of preconditioning via PKC translocation.
  • To assess the effects of PKC agonists and antagonists on cardiac contractile function following ischemia.

Main Methods:

  • Langendorff-perfused rabbit hearts were treated with control, vehicle, PKC agonists (acetylcholine, DOG), or a PKC antagonist (chelerythrine).
  • Hearts underwent a 2-hour ischemic period followed by 45-minute reperfusion.
  • PKC translocation was measured using an antibody against PKC delta isoforms, and metabolic changes were assessed via nucleotide, lactate, and pH levels.

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Main Results:

  • PKC agonists (DOG, acetylcholine) significantly improved recovery of developed pressure post-ischemia.
  • PKC delta isoforms translocated to the cell membrane during ischemia, an effect mimicked by DOG and blocked by chelerythrine.
  • No significant differences in pH, lactate, or nucleotide levels were observed between groups, indicating metabolic changes were not the primary driver.

Conclusions:

  • PKC translocation is a critical mechanism for improved post-ischemic cardiac function.
  • The protective effects are independent of alterations in cellular energetics or metabolism.
  • Targeting PKC translocation warrants further investigation for therapeutic strategies against myocardial ischemia.