FGF2-induced STAT3 activation regulates pathologic neovascularization

Zhenyu Dong, Andrea Santeford, Norimitsu Ban, Tae Jun Lee, Craig Smith, David M. Ornitz, Rajendra S. Apte

Research output: Contribution to journalArticle

1 Scopus citations

Abstract

Cell-autonomous endothelial cell (EC) fibroblast growth factor receptor (FGFR) signaling through FGFR1/2 is essential for injury-induced wound vascularization and pathologic neovascularization as in blinding eye diseases such as age-related macular degeneration. Which FGF ligand(s) is critical in regulating angiogenesis is unknown. Utilizing ex vivo models of choroidal endothelial sprouting and in vivo models of choroidal neovascularization (CNV), we demonstrate here that only FGF2 is the essential ligand. Though FGF-FGFR signaling can activate multiple intracellular signaling pathways, we show that FGF2 regulates pathogenic angiogenesis via STAT3 activation. The identification of FGF2 as a critical mediator in aberrant neovascularization provides a new opportunity for developing multi-target therapies in blinding eye diseases especially given the limitations of anti-VEGF monotherapy.

Original languageEnglish
Article number107775
JournalExperimental eye research
Volume187
DOIs
StatePublished - Oct 2019

Keywords

  • Choroid sprouting
  • Choroidal neovascularization
  • Endothelial cell
  • Fibroblast growth factor
  • Macular degeneration
  • Retina
  • STAT3

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