Transforming growth factor-beta inhibition reduces progression of early choroidal neovascularization lesions in rats: P17 and P144 peptides

PLoS One. 2013 May 31;8(5):e65434. doi: 10.1371/journal.pone.0065434. Print 2013.

Abstract

The purpose of this study was to assess the effects of transforming growth factor beta (TGF-β) inhibitor peptides (P17 & P144) on early laser-induced choroidal neovascularization (LI-CNV) lesions in rats, two weeks after laser CNV induction. Seventy-one Long Evans rats underwent diode laser application in an established LI-CNV model. Baseline fluorescein angiography (FA) was performed 14 days following laser procedure, and treatments were administered 16 days post-laser application via different administration routes. Intravenous groups included control (IV-Control), P17 (IV-17), and P144 (IV-144) groups, whereas intravitreal groups included P17 (IVT-17), P144 (IVT-144), and a mixture of both peptides (IVT-17+144) (with fellow eyes receiving vehicle alone). CNV evolution was assessed using FA performed weekly for four weeks after treatment. Following sacrifice, VEGF, TGF-β, COX-2, IGF-1, PAI-1, IL-6, MMP-2, MMP-9, and TNF-α gene expression was assessed using RT-PCR. VEGF and p-SMAD2 protein levels were also assessed by western-blot, while MMP-2 activity was assessed with gelatin zymography. Regarding the FA analysis, the mean CNV area was lower from the 3(rd) week in IVT-17 and IVT-144 groups, and also from the 2(nd) week in IVT-17+144. Biochemical analysis revealed that gene expression was lower for VEGF and COX-2 genes in IV-17 and IV-144 groups, VEGF gene in IVT-17+144 group and MMP-2 gene in IVT-17 and IVT-144 groups. VEGF protein expression was also decreased in IV-17, IV-144, IVT-17 and IVT-144, whereas pSMAD-2 levels were lower in IV-17, IV-144 and IVT-17+144 groups. Zymogram analysis revealed decreased MMP-2 activity in IV-17, IV-144, IVT-17 and IVT-144 groups. These data suggest that the use of TGF-β inhibitor peptides (P17 & P144) decrease the development of early CNV lesions by targeting different mediators than those typically affected using current anti-angiogenic therapies. Its potential role in the treatment of early CNV appears promising as a single therapy or adjuvant to anti-VEGF drugs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Choroidal Neovascularization / drug therapy
  • Choroidal Neovascularization / metabolism*
  • Choroidal Neovascularization / pathology*
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Disease Progression
  • Fluorescein Angiography
  • Gene Expression Regulation / drug effects
  • Male
  • Matrix Metalloproteinase 2 / metabolism
  • Peptide Fragments / administration & dosage
  • Peptide Fragments / pharmacology*
  • Peptides / administration & dosage
  • Peptides / pharmacology*
  • Phosphorylation / drug effects
  • Rats
  • Receptors, Transforming Growth Factor beta / administration & dosage
  • Smad2 Protein / metabolism
  • Transforming Growth Factor beta / antagonists & inhibitors
  • Transforming Growth Factor beta / metabolism*
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • P17 peptide
  • Peptide Fragments
  • Peptides
  • Receptors, Transforming Growth Factor beta
  • Smad2 Protein
  • TGF-beta1 type III receptor (730-743), human
  • Transforming Growth Factor beta
  • Vascular Endothelial Growth Factor A
  • Cyclooxygenase 2
  • Matrix Metalloproteinase 2

Grants and funding

This study was funded by Digna Biotech. The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript. Javier Dotor is an employee of Digna Biotech, and he established the formulation of peptide solutions for intravitreal and intravenous injections employed in the study and reviewed the methods section of the manuscript.