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Related Experiment Videos

Inositol polyphosphates regulate Ca2+ efflux in a cardiac membrane subtype distinct from junctional sarcoplasmic

E E Quist1, C W Quist, R Vasan

  • 1Department of Pharmacology, University of North Texas Health Science Center at Fort Worth 76107, USA. equist@hsc.unt.edu

Archives of Biochemistry and Biophysics
|January 9, 2001
PubMed
Summary
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Inositol 1,3,4,5-tetrakisphosphate (InsP4) regulates cardiac Ca2+ uptake via a distinct sarcoplasmic reticulum (SR) subtype. InsP4 and InsP3 modulate Ca2+ efflux through an ATP-sensitive channel in low-density SR.

Area of Science:

  • Cardiovascular Physiology
  • Cellular Signaling
  • Molecular Biology

Background:

  • Cardiac muscle function relies on precise calcium (Ca2+) handling within sarcoplasmic reticulum (SR) subtypes.
  • Inositol phosphates, including inositol 1,3,4,5-tetrakisphosphate (InsP4), are implicated in cellular signaling pathways.
  • The specific roles of InsP4 in regulating Ca2+ transport in cardiac membranes remain incompletely understood.

Purpose of the Study:

  • To investigate the membrane localization and mechanism of InsP4-regulated Ca2+ uptake in cardiac vesicles.
  • To differentiate the Ca2+ transport mechanisms in various SR subtypes.
  • To elucidate the role of InsP4 and other inositol phosphates in modulating Ca2+ flux.

Main Methods:

  • Canine and rat cardiac membrane vesicles were fractionated using sucrose density gradient centrifugation.

Related Experiment Videos

  • InsP4-regulated Ca2+ uptake and Ca2+ content were measured in different membrane fractions.
  • The effects of thapsigargin, ATP, InsP4 isomers, and ruthenium red on Ca2+ transport were assessed.

    • Main Results:

    • InsP4-regulated Ca2+ uptake was localized to low-density membranes enriched in type 1 InsP3 receptors.
    • Junctional SR (J-SR), rich in SERCA2a and ryanodine receptors, was found in higher-density membranes.
    • A high-affinity, thapsigargin-insensitive Ca2+ carrier mediated uptake in low-density SR, distinct from J-SR's SERCA2a.
    • ATP modulated Ca2+ efflux via an InsP3 receptor-like channel, with InsP4 enhancing or inhibiting uptake based on ATP concentration.
    • InsP4 and InsP3 stimulated Ca2+ efflux, with InsP4 being more potent.

    Conclusions:

    • A distinct SR subtype, separate from J-SR, utilizes a Ca2+ carrier for Ca2+ loading, regulated by InsP4.
    • InsP4 and InsP3 regulate Ca2+ efflux in low-density SR by acting on an ATP-modulated Ca2+ channel resembling type 1 InsP3 receptors.
    • This study reveals a novel mechanism for InsP4-mediated Ca2+ regulation in cardiac membranes, impacting Ca2+ homeostasis.