The effects of VEGF-R1 and VEGF-R2 ligands on angiogenic responses and left ventricular function in mice

Cardiovasc Res. 2010 Apr 1;86(1):122-30. doi: 10.1093/cvr/cvp382. Epub 2009 Dec 2.

Abstract

Aims: Vascular endothelial growth factors (VEGFs) and their receptors (VEGF-Rs) are among the most powerful factors regulating vascular growth. However, it has remained unknown whether stimulation of VEGF-R1, VEGF-R2 or both of the receptors produces the best angiogenic responses in myocardium. The aim of this study was to compare the VEGF-R1-specific ligand VEGF-B(186), VEGF-R2-specific ligand VEGF-E and VEGF-A(165,) which stimulates both receptors, regarding their effects on angiogenesis and left ventricular function in mice.

Methods and results: High-resolution echocardiography was used to guide the closed-chest injections of adenoviral (Ad) vectors expressing VEGF-B(186,) VEGF-E, and VEGF-A(165) into the anterior wall of the left ventricle in C57Bl/6J mice. Angiogenic and functional effects were analysed using histology, ultrasound and perfusion analyses 6 (D6) and 14 (D14) days after the Ad injection. AdVEGF-A(165) induced a strong angiogenic response seen as an enlargement of myocardial capillaries whereas angiogenesis induced by AdVEGF-B(186) and AdVEGF-E seemed more physiological. The increase in the capillary area was accompanied with an increase in myocardial perfusion at D6 after the gene injection. AdVEGF-A(165) and AdVEGF-E induced endothelial-specific proliferation whereas AdVEGF-B(186) mostly induced proliferation of cardiomyocytes. AdVEGF-A(165) induced more pronounced tissue damage than AdVEGF-B(186) and AdVEGF-E. Left ventricular function measured as ejection fraction did not change during the follow-up. AdVEGF-A(165) increased both VEGF-R1 and VEGF-R2 protein expression whereas AdVEGF-B(186) and AdVEGF-E did not affect endogenous receptor expression levels.

Conclusion: AdVEGF-B(186) and AdVEGF-E are equally potent in inducing therapeutic angiogenesis in mouse myocardium and produce less side effects than AdVEGF-A(165).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoviridae / genetics
  • Animals
  • Blotting, Western
  • Cell Division / drug effects
  • Cell Division / physiology
  • Coronary Circulation / drug effects
  • Coronary Circulation / physiology
  • Echocardiography
  • Enzyme-Linked Immunosorbent Assay
  • Ligands
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Models, Cardiovascular
  • Myocarditis / chemically induced
  • Myocarditis / metabolism
  • Myocarditis / physiopathology
  • Neovascularization, Physiologic / drug effects
  • Neovascularization, Physiologic / physiology*
  • Peptide Fragments / genetics
  • Peptide Fragments / metabolism
  • Peptide Fragments / pharmacology
  • Stroke Volume / drug effects
  • Stroke Volume / physiology
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / metabolism*
  • Vascular Endothelial Growth Factor A / pharmacology
  • Vascular Endothelial Growth Factor B / genetics
  • Vascular Endothelial Growth Factor B / metabolism
  • Vascular Endothelial Growth Factor B / pharmacology
  • Vascular Endothelial Growth Factor Receptor-1 / metabolism*
  • Vascular Endothelial Growth Factor Receptor-2 / metabolism*
  • Ventricular Function, Left / drug effects
  • Ventricular Function, Left / physiology*
  • Viral Proteins / genetics
  • Viral Proteins / metabolism
  • Viral Proteins / pharmacology

Substances

  • Ligands
  • Peptide Fragments
  • VEGF-like protein, Orf virus
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factor B
  • Viral Proteins
  • vascular endothelial growth factor A (138-165)
  • Vascular Endothelial Growth Factor Receptor-1
  • Vascular Endothelial Growth Factor Receptor-2