Abstract
In our study, we found cardiocytes expressed CXCR4, and the number of cardiocytes apoptosis with SDF-1 treatment decreased obviously through SDF-1 induced the up-regulation of phosphorylated Akt. On day 7 after myocardial infarction, marked expression of SDF-1alpha, and the number of CD133(+) cells was the highest in the AdV-SDF-1 injection hearts. On day 28 post-treatment, blood vessel density in the AdV. SDF-1 group was higher in infracted zones. Infarct size and collagen accumulation in the infracted area decreased significantly, thickness of LV wall, vessels and cardiocytes' density increased obviously in the AdV-SDF-1 group than in control or Adv-LacZ group, and hemodynamics showed the improvement of left ventricle heart function in the AdV.SDF-1 group. Therefore, SDF-1alpha could improve cardiac structure and function through the combined effects of angiogenesis and anti-apoptosis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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AC133 Antigen
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Adenoviridae / genetics*
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Animals
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Antigens, CD / metabolism
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Apoptosis*
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Cell Movement
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Cell Survival
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Chemokine CXCL12 / genetics
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Chemokine CXCL12 / metabolism*
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Collagen / metabolism
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Disease Models, Animal
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Endothelial Cells / metabolism
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Endothelial Cells / pathology
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Genetic Therapy / methods*
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Genetic Vectors*
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Glycoproteins / metabolism
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Humans
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Myocardial Infarction / genetics
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Myocardial Infarction / metabolism
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Myocardial Infarction / physiopathology
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Myocardial Infarction / therapy*
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Myocardium / immunology
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Myocardium / metabolism*
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Myocardium / pathology
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Myocytes, Cardiac / metabolism
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Myocytes, Cardiac / pathology
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Neovascularization, Physiologic*
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Peptides / metabolism
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Phosphorylation
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Proto-Oncogene Proteins c-akt / metabolism
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Rats
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Receptors, CXCR4 / metabolism
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Stem Cells / immunology
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Stem Cells / metabolism*
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Stem Cells / pathology
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Time Factors
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Ventricular Function, Left
Substances
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AC133 Antigen
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Antigens, CD
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CXCL12 protein, human
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Chemokine CXCL12
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Cxcr4 protein, rat
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Glycoproteins
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PROM1 protein, human
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Peptides
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Prom1 protein, rat
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Receptors, CXCR4
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Collagen
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Proto-Oncogene Proteins c-akt