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Related Experiment Videos

Sarcoplasmic reticulum membrane and heart development.

M Michalak

    The Canadian Journal of Cardiology
    |June 1, 1987
    PubMed
    Summary
    This summary is machine-generated.

    Cardiac sarcoplasmic reticulum function is immature in fetuses, with lower Ca2+ uptake and ATPase activity. These developmental differences in Ca2+ handling proteins explain fetal heart muscle

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    Area of Science:

    • Cardiovascular Biology
    • Muscle Physiology
    • Cellular Biochemistry

    Background:

    • Intracellular calcium (Ca2+) regulates cardiac cell function, involving trans-sarcolemmal fluxes and sarcoplasmic reticulum (SR) activity.
    • SR Ca2+ uptake causes relaxation, while Ca2+ release initiates contraction, mediated by Ca2+-dependent ATPase and potential ligand-gated channels.
    • The role of SR in developing muscle is not fully understood.

    Purpose of the Study:

    • Investigate the composition and function of SR membranes during cardiac myogenesis.
    • Characterize age-related differences in SR Ca2+ transport and protein content.
    • Correlate SR properties with intracellular Ca2+ regulation in fetal heart muscle.

    Main Methods:

    • Isolated SR vesicles from fetal and adult cardiac muscle.

    Related Experiment Videos

  • Assessed Ca2+ uptake and Ca2+-dependent ATPase activity.
  • Quantified Ca2+-ATPase and calsequestrin using specific antibodies.
  • Examined phospholamban phosphorylation by cAMP-dependent protein kinase.

    • Main Results:

    • Embryonic phospholamban was phosphorylated by cAMP-dependent protein kinase but not Ca2+/calmodulin.
    • Fetal SR exhibited lower Ca2+ uptake and Ca2+-dependent ATPase activity compared to adult SR.
    • Amounts of Ca2+-ATPase and calsequestrin were reduced in fetal SR.
    • SR vesicles showed minimal contamination from other cellular membranes.

    Conclusions:

    • Cardiac SR composition and function undergo significant changes during development.
    • Lower Ca2+ transport capacity and reduced protein levels in fetal SR contribute to altered intracellular Ca2+ regulation.
    • These findings help explain developmental changes in myocardial function and Ca2+ handling in the fetal heart.