TY - JOUR
T1 - Chronic treatment with clenbuterol modulates endothelial progenitor cells and circulating factors in a murine model of cardiomyopathy
AU - Rider, James E.
AU - Polster, Sean P.
AU - Lee, Sangjin
AU - Charles, Nathan J.
AU - Adhikari, Neeta
AU - Mariash, Ami
AU - Tadros, George
AU - Stangland, Jenna
AU - Smolenski, Ryszard T.
AU - Terracciano, Cesare M.
AU - Barton, Paul J.R.
AU - Birks, Emma J.
AU - Yacoub, Magdi H.
AU - Miller, Leslie W.
AU - Hall, Jennifer L.
PY - 2009/6
Y1 - 2009/6
N2 - 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.
AB - 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.
KW - Beta 2 adrenergic receptor
KW - Clenbuterol
KW - Endothelial progenitor cell
KW - Heart failure
KW - Muscle LIM protein
UR - https://www.scopus.com/pages/publications/67349140886
UR - https://www.scopus.com/pages/publications/67349140886#tab=citedBy
U2 - 10.1007/s12265-009-9089-6
DO - 10.1007/s12265-009-9089-6
M3 - Article
C2 - 20559986
AN - SCOPUS:67349140886
SN - 1937-5387
VL - 2
SP - 182
EP - 190
JO - Journal of Cardiovascular Translational Research
JF - Journal of Cardiovascular Translational Research
IS - 2
ER -