Involvement of Lgals3/Galectin-3 in Choroidal Neovascularization and Subretinal Fibrosis Formation

<b>Background:</b><i>Lgals3</i>/galectin-3 plays a pivotal role in many vascular diseases. However, the involvement of <i>Lgals3</i>/galectin-3 in eyes with neovascular age-related macular degeneration (nAMD) remains unknown. <b>Methods:</b> In the laser-induced CNV model, a whole mount retina stained with Isolectin B4 and collagen type I revealed the vascular bed and CNV-associated subretinal fibrosis on day 7 after laser treatment. <b>Results:</b> We show that the expression levels of <i>Lgals3</i>/galectin-3 were significantly increased in the RPE/choroidal complex of CNV mice. An intravitreal injection of <i>Lgals3</i>-siRNA significantly suppressed the area of CNV and subretinal fibrosis, together with <i>Mcp-1</i> decline. The mixture of <i>Lgals3</i>-siRNA and Ranibizumab showed more efficiency than each drug used separately. Hypoxia induced <i>Lgals3</i>/galectin-3 production in ARPE-19 cells, which was reduced by the silencing hypoxia-inducible factor -1α (<i>Hif-1a</i>). <b>Conclusions:</b> Our data indicated that <i>Lgals3</i>/galectin-3 is involved in the pathogenesis of CNV and subretinal fibrosis, and <i>Lgals3</i>/galectin-3 could be a potential therapeutic target for nAMD.