Sema3f Protects Against Subretinal Neovascularization In Vivo

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Sema3f Protects Against Subretinal Neovascularization In Vivo

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Title: Sema3f Protects Against Subretinal Neovascularization In Vivo
Author: Sun, Ye; Liegl, Raffael; Gong, Yan; Bühler, Anima; Cakir, Bertan; Meng, Steven S.; Burnim, Samuel B.; Liu, Chi-Hsiu; Reuer, Tristan; Zhang, Peipei; Walz, Johanna M.; Ludwig, Franziska; Lange, Clemens; Agostini, Hansjürgen; Böhringer, Daniel; Schlunck, Günther; Smith, Lois E.H.; Stahl, Andreas

Note: Order does not necessarily reflect citation order of authors.

Citation: Sun, 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.
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Abstract: 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.
Published Version: doi:10.1016/j.ebiom.2017.03.026
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