Department of Ophthalmology, University of Rochester, Rochester, NY 14620, USA; Department of Biomedical Genetics, University of Rochester, Rochester, NY 14620, USA.
Department of Ophthalmology, University of Rochester, Rochester, NY 14620, USA; Department of Biomedical Genetics, University of Rochester, Rochester, NY 14620, USA; Department of Pathology and Laboratory Medicine, University of Rochester, Rochester, NY 14620, USA.
Cell Stem Cell. 2021 May 6;28(5):846-862.e8. doi: 10.1016/j.stem.2021.02.006. Epub 2021 Mar 29.
The retinal pigment epithelium (RPE)-choriocapillaris (CC) complex in the eye is compromised in age-related macular degeneration (AMD) and related macular dystrophies (MDs), yet in vitro models of RPE-CC complex that enable investigation of AMD/MD pathophysiology are lacking. By incorporating iPSC-derived cells into a hydrogel-based extracellular matrix, we developed a 3D RPE-CC model that recapitulates key features of both healthy and AMD/MD eyes and provides modular control over RPE and CC layers. Using this 3D RPE-CC model, we demonstrated that both RPE- and mesenchyme-secreted factors are necessary for the formation of fenestrated CC-like vasculature. Our data show that choroidal neovascularization (CNV) and CC atrophy occur in the absence of endothelial cell dysfunction and are not necessarily secondary to drusen deposits underneath RPE cells, and CC atrophy and/or CNV can be initiated systemically by patient serum or locally by mutant RPE-secreted factors. Finally, we identify FGF2 and matrix metalloproteinases as potential therapeutic targets for AMD/MDs.
眼睛中的视网膜色素上皮 (RPE)-脉络膜毛细血管 (CC) 复合物在年龄相关性黄斑变性 (AMD) 和相关的黄斑营养不良 (MD) 中受损,但缺乏能够研究 AMD/MD 病理生理学的体外 RPE-CC 复合物模型。通过将 iPSC 衍生的细胞纳入基于水凝胶的细胞外基质中,我们开发了一种 3D RPE-CC 模型,该模型再现了健康和 AMD/MD 眼睛的关键特征,并对 RPE 和 CC 层进行了模块化控制。使用这种 3D RPE-CC 模型,我们证明了 RPE 和间充质分泌的因子对于形成有孔的 CC 样脉管系统都是必需的。我们的数据表明,脉络膜新生血管形成 (CNV) 和 CC 萎缩的发生并不一定是由于 RPE 细胞下方的脉络膜新生血管形成 (CNV) 功能障碍,也不一定是由于 RPE 细胞下方的脉络膜新生血管形成 (CNV) 功能障碍,也不一定是由于 RPE 细胞下方的 drusen 沉积所致,并且 CC 萎缩和/或 CNV 可以通过患者血清全身或局部由突变的 RPE 分泌因子引发。最后,我们确定 FGF2 和基质金属蛋白酶是 AMD/MD 的潜在治疗靶点。