Adenovirus-mediated stromal cell-derived- factor-1alpha gene transfer induces cardiac preservation after infarction via angiogenesis of CD133+ stem cells and anti-apoptosis

Interact Cardiovasc Thorac Surg. 2008 Oct;7(5):767-70. doi: 10.1510/icvts.2007.169896. Epub 2008 Jun 24.

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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • AC133 Antigen
  • Adenoviridae / genetics*
  • Animals
  • Antigens, CD / metabolism
  • Apoptosis*
  • Cell Movement
  • Cell Survival
  • Chemokine CXCL12 / genetics
  • Chemokine CXCL12 / metabolism*
  • Collagen / metabolism
  • Disease Models, Animal
  • Endothelial Cells / metabolism
  • Endothelial Cells / pathology
  • Genetic Therapy / methods*
  • Genetic Vectors*
  • Glycoproteins / metabolism
  • Humans
  • Myocardial Infarction / genetics
  • Myocardial Infarction / metabolism
  • Myocardial Infarction / physiopathology
  • Myocardial Infarction / therapy*
  • Myocardium / immunology
  • Myocardium / metabolism*
  • Myocardium / pathology
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology
  • Neovascularization, Physiologic*
  • Peptides / metabolism
  • Phosphorylation
  • Proto-Oncogene Proteins c-akt / metabolism
  • Rats
  • Receptors, CXCR4 / metabolism
  • Stem Cells / immunology
  • Stem Cells / metabolism*
  • Stem Cells / pathology
  • Time Factors
  • Ventricular Function, Left

Substances

  • AC133 Antigen
  • Antigens, CD
  • CXCL12 protein, human
  • Chemokine CXCL12
  • Cxcr4 protein, rat
  • Glycoproteins
  • PROM1 protein, human
  • Peptides
  • Prom1 protein, rat
  • Receptors, CXCR4
  • Collagen
  • Proto-Oncogene Proteins c-akt