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Dynamic expression of the membrane attack complex (MAC) of the complement system in failing human myocardium

Guilherme H M Oliveira1, Corinne N Brann, Katy Becker

  • 1Baylor College of Medicine, Houston, Texas; Methodist DeBakey Heart Center, Houston, Texas, USA.

The American Journal of Cardiology
|May 27, 2006
PubMed

Insights

The complement system

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Heart failure involves inflammatory cytokine pathways.
  • The complement system, producing the membrane attack complex (MAC), is a key inflammatory response.
  • MAC causes cell lysis and apoptosis.

Purpose of the Study:

  • To investigate complement system activation in heart failure.
  • To determine if hemodynamic conditions regulate MAC expression in the failing heart.

Main Methods:

  • Assessed MAC expression in myocardial biopsies from normal and failing hearts.
  • Utilized immunohistochemistry and Western blot analysis.
  • Analyzed samples before and after left ventricular assist device (LVAD) implantation.

Main Results:

  • Increased MAC expression was found in failing hearts, but not normal hearts.
  • MAC expression decreased to normal levels after hemodynamic unloading with LVAD support.
  • No difference in MAC expression was observed between ischemic and non-ischemic heart failure causes.

Conclusions:

  • The complement system is activated in the heart failure environment, evidenced by increased MAC expression.
  • Hemodynamic normalization dynamically regulates MAC expression, suggesting a pathogenic role.
  • The complement system represents a novel therapeutic target for heart failure.

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