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Cardioprotection through a PKC-dependent decrease in myofilament ATPase.

W Glen Pyle1, Yi Chen, Polly A Hofmann

  • 1Department of Physiology, University of Tennessee-Memphis, 894 Union Avenue, Memphis, TN 38163, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|May 24, 2003
PubMed
Summary
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Activation of kappa-opioid receptors protects the heart after ischemia by reducing energy use. Protein kinase C (PKC) activation and myofilament changes decrease ATP utilization, improving cardiac function.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Pharmacology

Background:

  • Myocardial kappa-opioid receptor (KOR) activation may offer cardioprotection.
  • Protein kinase C (PKC) pathways are implicated in cardiac function.
  • Reduced ATP utilization by myofilaments is a potential mechanism for cardioprotection.

Purpose of the Study:

  • To investigate the role of PKC in KOR-dependent cardioprotection.
  • To determine if KOR-PKC signaling reduces ATP utilization via myofilament effects.
  • To elucidate the molecular mechanisms linking KOR activation to improved postischemic cardiac function.

Main Methods:

  • Utilized KOR agonist U50,488H and PKC inhibitors in isolated heart models.
  • Assessed postischemic left ventricular developed pressure and end-diastolic pressure.

Related Experiment Videos

  • Measured actomyosin Mg2+-ATPase activity and quantified myofilament protein phosphorylation (PKC-epsilon, troponin I, C-protein) using immunoblotting and confocal microscopy.

    • Main Results:

    • KOR agonist U50,488H improved postischemic cardiac function.
    • PKC inhibitors abolished the cardioprotective effects of U50,488H.
    • Decreases in myofibrillar ATPase activity were cardioprotective.
    • KOR stimulation increased myofilament-associated PKC-epsilon and phosphorylation of troponin I and C-protein.

    Conclusions:

    • PKC activation is essential for KOR-dependent cardioprotection.
    • KOR-mediated cardioprotection involves decreased myofilament ATP utilization.
    • PKC-epsilon activation and translocation to myofilaments reduce actomyosin ATPase, contributing to KOR cardioprotective effects.