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Nitric oxide synthase in experimental autoimmune myocarditis dysfunction

N Goren1, C P Leiros, L Sterin-Borda

  • 1Centro de Estudios Farmacológicos y Botánicos (CEFYBO) and Cátedra de Farmacología de la Facultad de Odontología de la Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Argentina.

Journal of Molecular and Cellular Cardiology
|January 30, 1999
PubMed
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This study reveals that inducible nitric oxide synthase (iNOS) expression in autoimmune myocarditis hearts contributes to cardiac dysfunction. Treatments targeting iNOS or interferon-gamma improved heart contractility in affected mice.

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Molecular Biology

Background:

  • Autoimmune myocarditis can lead to cardiac dysfunction.
  • The role of inducible nitric oxide synthase (iNOS) in myocarditis-induced heart alterations is not fully understood.

Purpose of the Study:

  • To investigate the expression and role of iNOS in the cardiac dysfunction associated with autoimmune myocarditis.
  • To explore potential therapeutic targets for improving cardiac contractility in myocarditis.

Main Methods:

  • Assessing iNOS expression via [U-14C]citrulline production from [U-14C]arginine and immunoblot assays.
  • Evaluating the effects of dexamethasone, anti-interferon-gamma monoclonal antibody (anti-IFN-gamma mAb), and enzyme inhibitors (staurosporine, trifluoperazine) on iNOS activity and cardiac function.

Related Experiment Videos

  • Measuring atrial contractile function (dF/dt) in control and autoimmune myocarditis mice.

    • Main Results:

    • iNOS was expressed in autoimmune atria, where it is normally absent.
    • Dexamethasone and anti-IFN-gamma mAb administration reduced iNOS activity.
    • Inhibitors of protein kinase C, but not calcium/calmodulin, attenuated iNOS activity.
    • Autoimmune atria exhibited impaired contractile function (reduced dF/dt).
    • In vivo treatments with NOS inhibitors, anti-IFN-gamma mAb, or dexamethasone improved cardiac contractility in autoimmune mice.

    Conclusions:

    • Infiltrative cells in myocarditis hearts produce interferon-gamma (IFN-gamma), leading to iNOS expression and subsequent cardiac contractile dysfunction.
    • Activation of the L-arginine nitric oxide pathway by cytokines plays a critical role in myocarditis-associated contractile dysfunction.
    • Targeting the IFN-gamma/iNOS pathway and nitric oxide production represents a potential therapeutic strategy for autoimmune myocarditis.