TGF-β concentrations and activity are down-regulated in the aqueous humor of patients with neovascular age-related macular degeneration

Sci Rep. 2018 May 23;8(1):8053. doi: 10.1038/s41598-018-26442-0.

Abstract

Controversy still exists regarding the role of the TGF-β in neovascular age-related macular degeneration (nAMD), a major cause of severe visual loss in the elderly in developed countries. Here, we measured the concentrations of active TGF-β1, TGF-β2, and TGF-β3 by ELISA in the aqueous humor of 20 patients affected by nAMD, who received 3 consecutive monthly intravitreal injections of anti-VEGF-A antibody. Samples were collected at baseline (before the first injection), month 1 (before the second injection), and month 2 (before the third injection). The same samples were used in a luciferase-based reporter assay to test the TGF-β pathway activation. Active TGF-β1 concentrations in the aqueous humor were below the minimum detectable dose. Active TGF-β2 concentrations were significantly lower at baseline and at month 1, compared to controls. No significant differences in active TGF-β3 concentration were found among the sample groups. Moreover, TGF-β pathway activation was significantly lower at baseline compared to controls. Our data corroborate an anti-angiogenic role for TGF-β2 in nAMD. This should be considered from the perspective of a therapy using TGF-β inhibitors.

Publication types

  • Observational Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Angiogenesis Inhibitors / administration & dosage
  • Angiogenesis Inhibitors / pharmacology
  • Aqueous Humor / drug effects
  • Aqueous Humor / metabolism*
  • Case-Control Studies
  • Down-Regulation
  • Female
  • Gene Expression Regulation
  • Humans
  • Intravitreal Injections
  • Macular Degeneration / drug therapy
  • Macular Degeneration / metabolism*
  • Macular Degeneration / pathology
  • Male
  • Neovascularization, Pathologic / drug therapy
  • Neovascularization, Pathologic / metabolism*
  • Neovascularization, Pathologic / pathology
  • Ranibizumab / administration & dosage
  • Ranibizumab / pharmacology*
  • Transforming Growth Factor beta1 / metabolism*
  • Transforming Growth Factor beta2 / metabolism*
  • Transforming Growth Factor beta3 / metabolism*
  • Vascular Endothelial Growth Factor A / antagonists & inhibitors

Substances

  • Angiogenesis Inhibitors
  • TGFB1 protein, human
  • TGFB2 protein, human
  • TGFB3 protein, human
  • Transforming Growth Factor beta1
  • Transforming Growth Factor beta2
  • Transforming Growth Factor beta3
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • Ranibizumab