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Atrial expression of the CCN1 and CCN2 proteins in chronic heart failure

Tomasz A Bonda1, Karol A Kamiński, Magdalena Dziemidowicz

  • 1Department of General and Experimental Pathology, Medical University of Bialystok, Mickiewicza Str. 2c, 15-222 Bialystok, Poland. tomasz.bonda@umb.edu.pl

Folia Histochemica Et Cytobiologica
|April 26, 2012
PubMed

Insights

In chronic heart failure, CCN1 protein increases in the atria, while CCN2 levels decrease. Angiotensin II signaling influences these CCN protein changes, suggesting a role in heart failure.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Biochemistry

Background:

  • CCN proteins (CCN1 and CCN2) are implicated in cellular responses to injury.
  • Previous research indicates CCN protein upregulation following acute cardiac damage.
  • The role of CCN proteins in chronic heart failure, particularly in atrial tissue, remains less understood.

Purpose of the Study:

  • To investigate the expression of CCN1 and CCN2 proteins in the atrial myocardium of mice with chronic heart failure.
  • To determine the regulatory role of angiotensin II in atrial CCN protein expression during heart failure.
  • To compare findings in mice with human atrial tissue to assess translational relevance.

Main Methods:

  • Myocardial infarction (MI) model in adult male mice, with or without telmisartan treatment (AT1 receptor antagonist).
  • Sham-operated mice served as controls.
  • Immunohistochemistry was used to evaluate CCN1 and CCN2 protein expression in atrial cardiomyocytes 12 weeks post-MI.
  • Human right atrial appendages were analyzed for comparison.

Main Results:

  • Constitutive expression of CCN1 and CCN2 was observed in atrial cardiomyocytes of control mice.
  • Myocardial infarction led to CCN1 upregulation and maintained CCN2 at basal levels in atrial tissue.
  • Telmisartan treatment prevented CCN1 upregulation and reduced CCN2 levels.
  • A non-significant inverse correlation between CCN1/CCN2 levels and left ventricular ejection fraction was found in human atrial samples.

Conclusions:

  • CCN1 and CCN2 proteins are constitutively expressed in murine atria.
  • Chronic heart failure is associated with altered CCN protein expression, with a tendency towards CCN1 upregulation.
  • Angiotensin II signaling, via the AT1 receptor, appears to modulate CCN1 and CCN2 expression in the atrial myocardium during heart failure.
  • Findings suggest a conserved atrial regulation of CCN proteins in both mice and humans, potentially linked to heart failure pathogenesis.

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