Sema3f Protects Against Subretinal Neovascularization In Vivo
Meng, Steven S.
Burnim, Samuel B.
Walz, Johanna M.
Smith, Lois E.H.
Stahl, AndreasNote: Order does not necessarily reflect citation order of authors.
MetadataShow full item record
CitationSun, Y., R. Liegl, Y. Gong, A. Bühler, B. Cakir, S. S. Meng, S. B. Burnim, et al. 2017. “Sema3f Protects Against Subretinal Neovascularization In Vivo.” EBioMedicine 18 (1): 281-287. doi:10.1016/j.ebiom.2017.03.026. http://dx.doi.org/10.1016/j.ebiom.2017.03.026.
AbstractPathological 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.
Citable link to this pagehttp://nrs.harvard.edu/urn-3:HUL.InstRepos:33029780
- HMS Scholarly Articles