Journal of Cardiovascular Translational Research

, Volume 2, Issue 2, pp 182–190

Chronic Treatment with Clenbuterol Modulates Endothelial Progenitor Cells and Circulating Factors in a Murine Model of Cardiomyopathy

Authors

  • James E. Rider
    • Lillehei Heart InstituteUniversity of Minnesota
  • Sean P. Polster
    • Lillehei Heart InstituteUniversity of Minnesota
  • Sangjin Lee
    • Lillehei Heart InstituteUniversity of Minnesota
  • Nathan J. Charles
    • Lillehei Heart InstituteUniversity of Minnesota
  • Neeta Adhikari
    • Lillehei Heart InstituteUniversity of Minnesota
  • Ami Mariash
    • Lillehei Heart InstituteUniversity of Minnesota
  • George Tadros
    • Lillehei Heart InstituteUniversity of Minnesota
  • Jenna Stangland
    • Lillehei Heart InstituteUniversity of Minnesota
  • Ryszard T. Smolenski
    • Heart Science Centre, National Heart and Lung InstituteImperial College London
  • Cesare M Terracciano
    • Heart Science Centre, National Heart and Lung InstituteImperial College London
  • Paul J.R. Barton
    • Heart Science Centre, National Heart and Lung InstituteImperial College London
  • Emma J. Birks
    • Heart Science Centre, National Heart and Lung InstituteImperial College London
  • Magdi H. Yacoub
    • Heart Science Centre, National Heart and Lung InstituteImperial College London
  • Leslie W. Miller
    • Washington Hospital Center and Georgetown University
    • Lillehei Heart InstituteUniversity of Minnesota
Article

DOI: 10.1007/s12265-009-9089-6

Cite this article as:
Rider, J.E., Polster, S.P., Lee, S. et al. J. of Cardiovasc. Trans. Res. (2009) 2: 182. doi:10.1007/s12265-009-9089-6

Abstract

The purpose of this study was to determine the effects of chronic treatment with the beta 2 adrenergic receptor agonist clenbuterol on endothelial progenitor cells (EPC) in a well-characterized model of heart failure, the muscle LIM protein knockout (MLP−/−) mouse. MLP−/− mice were treated daily with clenbuterol (2 mg/kg) or saline subcutaneously for 6 weeks. Clenbuterol led to a 30% increase in CD31+ cells in the bone marrow of MLP−/− heart failure mice (p < 0.004). Clenbuterol did not improve ejection fraction. Clenbuterol treatment in MLP−/− mice was associated with significant changes in the following circulating factors: tissue inhibitor of metalloproteinase-type 1, leukemia inhibitory factor 1, C-reactive protein, apolipoprotein A1, fibroblast growth factor 2, serum glutamic oxaloacetic transaminase, macrophage-derived chemokine, and monocyte chemoattractant protein-3. Clenbuterol treatment in the MLP−/− model of heart failure did not rescue heart function, yet did increase CD31+ cells in the bone marrow. This is the first evidence that a beta 2 agonist increases EPC proliferation in the bone marrow in a preclinical model of heart failure.

Keywords

ClenbuterolHeart FailureMuscle LIM ProteinBeta 2 Adrenergic ReceptorEndothelial Progenitor Cell

Copyright information

© Springer Science+Business Media, LLC 2009