Chronic treatment with clenbuterol modulates endothelial progenitor cells and circulating factors in a murine model of cardiomyopathy

James E. Rider, Sean P. Polster, Sangjin Lee, Nathan J. Charles, Neeta Adhikari, Ami Mariash, George Tadros, Jenna Stangland, Ryszard T. Smolenski, Cesare M. Terracciano, Paul J.R. Barton, Emma J. Birks, Magdi H. Yacoub, Leslie W. Miller, Jennifer L Hall

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)182-190
Number of pages9
JournalJournal of cardiovascular translational research
Volume2
Issue number2
DOIs
StatePublished - Jun 2009

Keywords

  • Beta 2 adrenergic receptor
  • Clenbuterol
  • Endothelial progenitor cell
  • Heart failure
  • Muscle LIM protein

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