Galectin‐1 promotes choroidal neovascularization and subretinal fibrosis mediatedviaepithelialmesenchymal transition

• DOI: 10.1096/fj.201801227r
• Publication Date: 2018-10-02T19:49:40Z
• Authors: Di Wu; Atsuhiro Kanda; Ye Liu; Satoru Kase; Kousuke Noda; Susumu Ishida
• Keywords: Galectin-3; Galectin-1

VEGFA and TGF-β are known major angiogenic fibrogenic factors. Galectin-1, encoded by lectin, galactoside-binding, soluble (LGALS)1, has attracted growing attention for its facilitatory role in angiogenesis fibrosis through modification of receptor signaling pathways. We reveal galectin-1 involvement the mouse model laser-induced choroidal neovascularization (CNV) subretinal fibrosis, both which represent pathogenesis age-related macular degeneration (AMD). Neither deletion nor overexpression Lgals1 affected physiologic retinal development or visual function. Galectin-1/Lgals1 was upregulated CNV induction, whereas suppressed together with downstream molecules VEGF (VEGFR)2. Loss also attenuated expression epithelial-mesenchymal transition (EMT) markers including Snai1, phosphorylation SMAD family member 2. Supporting these vivo findings, silencing LGALS1 human pigment epithelial (RPE) cells inhibited TGF-β1-induced EMT-related cell motilities. Conversely, enhanced fibrosis. Specimens from patients AMD demonstrated colocalization VEGFR2 neovascular endothelial phosphorylated SMAD2 RPE cells. These results suggested a biologic significance as key promotor eyes AMD.—Wu, D., Kanda, A., Liu, Y., Kase, S., Noda, K., Ishida, S. Galectin-1 promotes mediated via epithelialmesenchymal transition. FASEB J. 33, 2498–2513 (2019). www.fasebj.org