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

Autor: Ryszard T. Smolenski, Paul J.R. Barton, James E. Rider, Sangjin Lee, Cesare M. Terracciano, Nathan J. Charles, George M Tadros, Ami Mariash, Emma J. Birks, Jenna Stangland, Leslie W. Miller, Magdi H. Yacoub, Neeta Adhikari, Jennifer L. Hall, Sean P. Polster
Rok vydání: 2009
Předmět:
Male
Chemokine
Time Factors
Carboxypeptidases A
Muscle Proteins
Pharmaceutical Science
Leukemia Inhibitory Factor
Ventricular Function
Left
Mice
Genetics (clinical)
Mice
Knockout
Stem Cells
Adrenergic beta-Agonists
LIM Domain Proteins
Platelet Endothelial Cell Adhesion Molecule-1
C-Reactive Protein
medicine.anatomical_structure
Clenbuterol
Molecular Medicine
Fibroblast Growth Factor 2
Cardiomyopathies
Cardiology and Cardiovascular Medicine
medicine.drug
Agonist
medicine.medical_specialty
medicine.drug_class
Injections
Subcutaneous
Biology
Endothelial progenitor cell
Article
Internal medicine
Genetics
medicine
Animals
Aspartate Aminotransferases
RNA
Messenger
Progenitor cell
Adrenergic beta-2 Receptor Agonists
Cell Proliferation
Chemokine CCL22
Tissue Inhibitor of Metalloproteinase-1
Apolipoprotein A-I
Myocardium
Monocyte
Endothelial Cells
Stroke Volume
medicine.disease
Mice
Inbred C57BL
Disease Models
Animal
Endocrinology
Gene Expression Regulation
Heart failure
biology.protein
Receptors
Adrenergic
beta-2
Bone marrow
Biomarkers
Zdroj: Journal of Cardiovascular Translational Research. 2:182-190
ISSN: 1937-5395
1937-5387
DOI: 10.1007/s12265-009-9089-6
Popis: 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.
Databáze: OpenAIRE
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