Lab for Stem Cell & Retinal Regeneration, Institute of Stem Cell Research, Division of Ophthalmic Genetics, The Eye Hospital, Wenzhou Medical University, State Key Laboratory of Ophthalmology, Optometry and Visual Science, Wenzhou 325027, China.
Hefei National Laboratory for Physical Sciences at Microscale, CAS Key Laboratory of Brain Function and Disease, Neurodegenerative Disorder Research Center, School of Life Sciences, University of Science and Technology of China, Hefei 230026, China.
Stem Cell Reports. 2018 Apr 10;10(4):1267-1281. doi: 10.1016/j.stemcr.2018.02.003. Epub 2018 Mar 8.
Retinitis pigmentosa (RP) is an irreversible, inherited retinopathy in which early-onset nyctalopia is observed. Despite the genetic heterogeneity of RP, RPGR mutations are the most common causes of this disease. Here, we generated induced pluripotent stem cells (iPSCs) from three RP patients with different frameshift mutations in the RPGR gene, which were then differentiated into retinal pigment epithelium (RPE) cells and well-structured retinal organoids possessing electrophysiological properties. We observed significant defects in photoreceptor in terms of morphology, localization, transcriptional profiling, and electrophysiological activity. Furthermore, shorted cilium was found in patient iPSCs, RPE cells, and three-dimensional retinal organoids. CRISPR-Cas9-mediated correction of RPGR mutation rescued photoreceptor structure and electrophysiological property, reversed the observed ciliopathy, and restored gene expression to a level in accordance with that in the control using transcriptome-based analysis. This study recapitulated the pathogenesis of RPGR using patient-specific organoids and achieved targeted gene therapy of RPGR mutations in a dish as proof-of-concept evidence.
色素性视网膜炎(RP)是一种不可逆转的遗传性视网膜病变,其早期发病特征为夜盲症。尽管 RP 存在遗传异质性,但 RPGR 基因突变是导致该疾病的最常见原因。在此,我们从三个具有 RPGR 基因突变的 RP 患者中生成了诱导多能干细胞(iPSC),然后将其分化为具有电生理特性的视网膜色素上皮(RPE)细胞和结构良好的视网膜类器官。我们观察到在形态、定位、转录谱和电生理活性方面,视杆细胞存在显著缺陷。此外,在患者 iPSC、RPE 细胞和三维视网膜类器官中均发现了短纤毛。CRISPR-Cas9 介导的 RPGR 突变校正挽救了视杆细胞的结构和电生理特性,逆转了观察到的纤毛病,并通过基于转录组的分析,将基因表达恢复到与对照一致的水平。本研究使用患者特异性类器官再现了 RPGR 的发病机制,并在体外实现了针对 RPGR 突变的靶向基因治疗,为该方法提供了概念验证依据。