期刊
JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH
卷 2, 期 2, 页码 182-190出版社
SPRINGER
DOI: 10.1007/s12265-009-9089-6
关键词
Clenbuterol; Heart Failure; Muscle LIM Protein; Beta 2 Adrenergic Receptor; Endothelial Progenitor Cell
资金
- NIDDK NIH HHS [R21 DK078029] Funding Source: Medline
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.
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