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Protein phosphatases decrease sarcoplasmic reticulum calcium content by stimulating calcium release in cardiac

Dmitry Terentyev1, Serge Viatchenko-Karpinski, Inna Gyorke

  • 1Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430-6551, USA.

The Journal of Physiology
|August 5, 2003
PubMed
Summary
This summary is machine-generated.

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Increased protein phosphatase activity in heart cells triggers calcium release, depleting stores and potentially contributing to heart failure. This study investigates phosphatases PP1 and PP2A

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Cellular Signaling

Background:

  • Protein phosphorylation/dephosphorylation regulates cardiac excitation-contraction coupling.
  • Aberrant kinase and phosphatase activity is linked to heart failure.
  • Mechanisms of phosphatases on intracellular Ca2+ handling are poorly understood.

Purpose of the Study:

  • To investigate the effects of protein phosphatases PP1 and PP2A on cardiac myocyte Ca2+ handling.
  • To elucidate the role of these phosphatases in regulating spontaneous Ca2+ sparks and sarcoplasmic reticulum (SR) Ca2+ load.

Main Methods:

  • Studied permeabilized cardiac myocytes.
  • Assessed Ca2+ sparks and SR Ca2+ load using caffeine application.
  • Utilized phosphatase inhibitors (okadaic acid, calyculin A).

Related Experiment Videos

  • Examined ryanodine receptors (RyRs) at the single channel level in lipid bilayers.
  • Confirmed RyR dephosphorylation via quantitative immunoblotting.

    • Main Results:

    • Exposure to PP1 or PP2A increased Ca2+ spark frequency, followed by event disappearance.
    • These changes correlated with SR Ca2+ store depletion.
    • Inhibitors prevented PP1/PP2A-induced alterations in Ca2+ release and SR Ca2+ load.
    • PP1 increased the open probability of RyRs in lipid bilayers.
    • Biochemical assays confirmed PP1-mediated RyR dephosphorylation.

    Conclusions:

    • Increased intracellular phosphatase activity stimulates RyR-mediated SR Ca2+ release.
    • This stimulation leads to depleted SR Ca2+ stores in cardiac myocytes.
    • Findings provide insights into phosphatase roles in cardiac Ca2+ handling and heart failure.