Fight against Angiogenesis-Related Blindness Laboratory, Department of Ophthalmology, College of Medicine, Seoul National University & Seoul Artificial Eye Center Clinical Research Institute, Seoul National University Hospital, 28 Yongon-dong, Chongno-gu, Seoul 110-744, Republic of Korea.
Biomaterials. 2011 Mar;32(7):1865-71. doi: 10.1016/j.biomaterials.2010.11.030. Epub 2010 Dec 9.
The pathological angiogenesis in the retina is the major cause of vision loss at all ages. In particular, retinopathy of prematurity (ROP) is a leading cause of blindness in children. This study investigated whether gold nanoparticle (GNP) could inhibit retinal neovascularization in the animal model of ROP. Intravitreal injection of GNP significantly inhibited retinal neovascularization in the mouse model of ROP. In addition, GNP effectively suppressed VEGF-induced in vitro angiogenesis of retinal microvascular endothelial cells including proliferation, migration and capillary-like networks formation. GNP blocked VEGF-induced auto-phosphorylation of VEGFR-2 to inhibit consequently ERK 1/2 activation. GNP never affected on the cellular viability of retinal microvascular endothelial cells and induced no retinal toxicity. Our data suggest that GNP could be a potent inhibitor to retinal neovascularization without retinal toxicity. Furthermore, GNP could be extensively applied to variable vaso-proliferative retinopathies mediated by VEGF.
视网膜病理性血管生成是导致各年龄段视力丧失的主要原因。特别是早产儿视网膜病变（ROP）是儿童失明的主要原因。本研究探讨了金纳米颗粒（GNP）是否可以抑制 ROP 动物模型中的视网膜新生血管形成。玻璃体内注射 GNP 可显著抑制 ROP 小鼠模型中的视网膜新生血管形成。此外，GNP 可有效抑制 VEGF 诱导的视网膜微血管内皮细胞体外血管生成，包括增殖、迁移和毛细血管样网络形成。GNP 阻断了 VEGF 诱导的 VEGFR-2 自身磷酸化，从而抑制了 ERK1/2 的激活。GNP 从不影响视网膜微血管内皮细胞的细胞活力，也不会引起视网膜毒性。我们的数据表明，GNP 可以作为一种有效的抑制视网膜新生血管形成的药物，而不会产生视网膜毒性。此外，GNP 可广泛应用于 VEGF 介导的各种血管增生性视网膜病变。
