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Inhibition of vascular permeability factor (vascular endothelial growth factor) with antipeptide antibodies

T M Sioussat1, H F Dvorak, T A Brock

  • 1Department of Pathology, Beth Israel Hospital, Boston, Massachusetts.

Insights

Antibodies targeting the N- and C-termini of vascular permeability factor (VPF), also known as vascular endothelial cell growth factor (VEGF), effectively block its ability to increase vascular permeability and stimulate cell growth.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Vascular permeability factor (VPF), or vascular endothelial cell growth factor (VEGF), is a protein secreted by various cells.
  • VPF/VEGF increases microvascular permeability, contributing to tumor fluid accumulation and angiogenesis.
  • It also acts as a mitogen for endothelial cells, crucial for vascular health.

Purpose of the Study:

  • To develop antibodies against VPF/VEGF to investigate its structure and function.
  • To determine which regions of VPF/VEGF are accessible in its native form.
  • To evaluate the functional impact of blocking specific VPF/VEGF regions.

Main Methods:

  • Antibodies were generated against synthetic peptides from the human VPF/VEGF sequence.
  • Antibody binding was tested against native and denatured/reduced VPF/VEGF.
  • The effect of antibodies on VPF/VEGF permeability, endothelial cell growth, and cytosolic calcium levels was assessed.

Main Results:

  • Antibodies to N- and C-terminal peptides bound both native and denatured VPF/VEGF.
  • Antibodies to internal peptides primarily bound denatured VPF/VEGF, indicating N- and C-termini exposure.
  • N- and C-terminal antibodies individually partially blocked VPF/VEGF activity; combined, they blocked nearly all activity.
  • These antibodies also inhibited VPF/VEGF-stimulated endothelial cell growth and calcium increase.

Conclusions:

  • The N- and C-termini of VPF/VEGF are exposed in solution.
  • Targeting these terminal regions with antibodies can effectively neutralize VPF/VEGF's biological activities.
  • This suggests a potential therapeutic strategy for conditions involving VPF/VEGF dysregulation.

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