EBioMedicine (Apr 2017)

Sema3f Protects Against Subretinal Neovascularization In Vivo

  • Ye Sun,
  • Raffael Liegl,
  • Yan Gong,
  • Anima Bühler,
  • Bertan Cakir,
  • Steven S. Meng,
  • Samuel B. Burnim,
  • Chi-Hsiu Liu,
  • Tristan Reuer,
  • Peipei Zhang,
  • Johanna M. Walz,
  • Franziska Ludwig,
  • Clemens Lange,
  • Hansjürgen Agostini,
  • Daniel Böhringer,
  • Günther Schlunck,
  • Lois E.H. Smith,
  • Andreas Stahl

DOI
https://doi.org/10.1016/j.ebiom.2017.03.026
Journal volume & issue
Vol. 18, no. C
pp. 281 – 287

Abstract

Read online

Pathological neovascularization of the outer retina is the hallmark of neovascular age-related macular degeneration (nAMD). Building on our previous observations that semaphorin 3F (Sema3f) is expressed in the outer retina and demonstrates anti-angiogenic potential, we have investigated whether Sema3f can be used to protect against subretinal neovascularization in two mouse models. Both in the very low-density lipid-receptor knockout (Vldlr−/−) model of spontaneous subretinal neovascularization as well as in the mouse model of laser-induced choroidal neovascularization (CNV), we found protective effects of Sema3f against the formation of pathologic neovascularization. In the Vldlr−/− model, AAV-induced overexpression of Sema3f reduced the size of pathologic neovascularization by 56%. In the laser-induced CNV model, intravitreally injected Sema3f reduced pathologic neovascularization by 30%. Combined, these results provide the first evidence from two distinct in vivo models for a use of Sema3f in protecting the outer retina against subretinal neovascularization.

Keywords