| First Author | Sun Y | Year | 2017 |
| Journal | EBioMedicine | Volume | 18 |
| Pages | 281-287 | PubMed ID | 28373097 |
| Mgi Jnum | J:277066 | Mgi Id | MGI:6296066 |
| Doi | 10.1016/j.ebiom.2017.03.026 | Citation | Sun Y, et al. (2017) Sema3f Protects Against Subretinal Neovascularization In Vivo. EBioMedicine 18:281-287 |
| abstractText | 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. |
