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Reduced myocardial expression of calcium handling protein in patients with severe chronic mitral regurgitation

Przemysław Leszek1, Jerzy Korewicki, Anna Klisiewicz

  • 1Institute of Cardiology, Alpejska 42 St., 04-628 Warsaw, Poland. leszekp@ikard.pl

European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery
|September 26, 2006
PubMed

Insights

In chronic severe mitral regurgitation, sarcoplasmic reticulum Ca2+-ATPase 2 (SERCA2) gene expression and protein levels are significantly reduced in the left ventricle. This down-regulation correlates with left ventricular remodeling, impacting heart function.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Left ventricle (LV) function is critical in mitral regurgitation (MR), but cellular mechanisms of LV remodeling in chronic severe MR remain unclear.
  • Defective intracellular Ca2+ handling, particularly sarcoplasmic reticulum Ca2+-ATPase 2 (SERCA2) activity, is implicated in impaired myocyte contraction and relaxation.

Purpose of the Study:

  • To investigate alterations in SERCA2 gene expression in the LV during remodeling secondary to chronic severe MR.

Main Methods:

  • LV samples from 12 patients with chronic severe MR and LV remodeling were analyzed.
  • SERCA2 isoforms (SERCA2a, SERCA2b) mRNA levels were quantified using RT-PCR.
  • SERCA2 protein levels were determined by Western blot.
  • Results were compared to non-failing human hearts (NFH).

Main Results:

  • Significant reductions in SERCA2a (-40%) and SERCA2b (-49%) mRNA levels were observed in MR patients compared to NFH.
  • SERCA2 protein levels were decreased by 38% in MR patients.
  • Correlations were found between SERCA2 isoforms mRNA and protein levels, and a negative correlation between SERCA2 protein and LV diastolic diameter was noted.

Conclusions:

  • Chronic volume overload in severe MR leads to down-regulation of SERCA2 at both mRNA and protein levels.
  • Reduced SERCA2 protein levels correlate with LV diastolic dilatation, suggesting a role in LV remodeling.
Abstract

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