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 language | English (US) |
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Pages (from-to) | 182-190 |
Number of pages | 9 |
Journal | Journal of cardiovascular translational research |
Volume | 2 |
Issue number | 2 |
DOIs | |
State | Published - Jun 2009 |
Keywords
- Beta 2 adrenergic receptor
- Clenbuterol
- Endothelial progenitor cell
- Heart failure
- Muscle LIM protein