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Sarcoplasmic reticulum Ca2+ load in human heart failure.

Burkert Pieske1, Lars S Maier, Stephan Schmidt-Schweda

  • 1Labor für Molekulare Kardiologie und Herzmuskelphysiologie, Abteilung Kardiologie und Angiologie, Georg-August-Universität Göttingen, Robert-Koch-Str. 40, 37085 Göttingen, Germany. pieske@med.uni-goettingen.de

Basic Research in Cardiology
|December 14, 2002
PubMed
Summary
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Heart failure alters sarcoplasmic reticulum (SR) calcium handling, reducing SR calcium content due to lower SERCA2a protein expression. Enhancing SERCA function may improve cardiac contractility in heart failure.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Physiology

Background:

  • Excitation-contraction coupling and intracellular calcium (Ca2+) homeostasis are critical for cardiac function.
  • These processes are significantly altered in heart failure, impacting cardiac contractility.

Purpose of the Study:

  • To investigate if altered Ca2+ handling by the sarcoplasmic reticulum (SR) contributes to heart failure.
  • To examine the relationship between SR Ca2+ handling, contractile function, and protein expression in failing human myocardium.

Main Methods:

  • Isolated human trabeculae from failing (NYHA IV) and nonfailing hearts were electrically stimulated.
  • Isometric twitch tension, intracellular Ca2+ transients, and SR Ca2+ content were measured under varying rest intervals.
  • Protein expression of SERCA2a and phospholamban (PLB) was analyzed using Western blot.

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Main Results:

  • Failing myocardium showed reduced post-rest potentiation compared to nonfailing, indicating impaired SR Ca2+ handling.
  • Lower SERCA2a protein expression and a reduced SERCA2a/PLB ratio were observed in failing trabeculae with impaired contractile recovery.
  • Overexpression of SERCA1 improved contractile function and relaxation in failing human myocytes.

Conclusions:

  • Sarcoplasmic reticulum Ca2+ handling is severely compromised in human heart failure.
  • Reduced SR Ca2+ release, linked to diminished SR Ca2+ content, is associated with depressed SERCA2a protein expression.
  • Strategies to enhance SERCA function or expression hold therapeutic potential for improving cardiac function in heart failure.