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European Journal of Heart Failure 2009 11(1):6-13; doi:10.1093/eurjhf/hfn002
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Beneficial effect of rosuvastatin on cardiac dysfunction is associated with alterations in calcium-regulatory proteins

Ying Yang1,{dagger}, Yun Mou1,{dagger}, Shen-Jiang Hu1,2,* and Michael Fu3

1 Institute of Cardiology, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou 310003, P.R. China
2 Division of Nitric Oxide and Inflammatory Medicine, E-Institute of Shanghai Universities, Shanghai, P.R. China
3 Heart Failure Center, Department of Medicine, Sahlgrenska University Hospital/Sahlgrenska, Gothenburg, Sweden

* Corresponding author. Tel: +86 571 85519933, Fax: +86 571 88828822. Email: s0hu0001{at}hotmail.com


  Abstract

Aims: The normal expression of Ca2+-regulatory protein is critical for efficient myocardial function. The present study tested the hypothesis that rosuvastatin treatment may attenuate left ventricular (LV) remodelling and dysfunction in the failing heart, which may be associated with alterations of Ca2+-regulatory protein.

Methods and results: We investigated the change of LV remodelling and function in a rat model of cardiac dysfunction due to myocardial infarction (MI) with or without rosuvastatin (10 mg/kg/day) treatment for 10 weeks. The protein expression of sarcoplasmic reticulum Ca2+ ATPase (SERCA)2a, phospholamban (PLB), and phospho-PLB at serine-16 (pSer16-PLB), as well as SERCA activity, interleukin (IL)-6, and IL-10 levels were evaluated. After rosuvastatin treatment, LV remodelling and dysfunction were prevented. Rosuvastatin prevented the decrease of SERCA2a and pSer16-PLB expression, increased SERCA activity, but showed no effect on PLB expression. Furthermore, rosuvastatin reduced the increased IL-6 level and further elevated IL-10 level in the peri-infarct and remote zones of MI. Serum lipid levels remained unchanged.

Conclusion: Rosuvastatin is effective in preventing LV remodelling and dysfunction in the failing heart. The molecular mechanism may be related to normalization of SERCA2a expression, SERCA activity, and pSer16-PLB levels, as well as through cytokine alterations independent of its lipid-lowering effect.

Key Words: Rosuvastatin • Myocardial infarction • Cardiac dysfunction • Sarcoplasmic reticulum Ca2+ ATPase • Phospholamban • Interleukin

Received November 30, 2007; Revised August 28, 2008; Accepted September 12, 2008

{dagger} Both authors contributed equally to this work.


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