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一体化腺相关病毒介导的Nrl基因失活挽救了Pde6a小鼠的视网膜变性。

All-in-one AAV-mediated Nrl gene inactivation rescues retinal degeneration in Pde6a mice.

作者信息

Liu Zhiquan, Chen Siyu, Lo Chien-Hui, Wang Qing, Sun Yang

机构信息

Department of Ophthalmology, Stanford University School of Medicine, Palo Alto, California, USA.

Palo Alto Veterans Administration, Palo Alto, California, USA.

出版信息

JCI Insight. 2024 Dec 20;9(24):e178159. doi: 10.1172/jci.insight.178159.

Abstract

Retinitis pigmentosa (RP) is a complex group of inherited retinal diseases characterized by progressive death of photoreceptor cells and eventual blindness. Pde6a, which encodes a cGMP-specific phosphodiesterase, is a crucial pathogenic gene for autosomal recessive RP (RP43); there is no effective therapy for this form of RP. The compact CRISPR/Staphylococcus aureus Cas9 (CRISPR/SaCas9) system, which can be packaged into a single adeno-associated virus (AAV), holds promise for simplifying effective gene therapy. Here, we demonstrated that all-in-one AAV-SaCas9-mediated Nrl gene inactivation can efficiently prevent retinal degeneration in a RP mouse model with Pde6anmf363/nmf363 mutation. We screened single-guide RNAs capable of efficiently editing the mouse Nrl gene in N2a cells and then achieved effective gene editing by using a single AAV to codeliver SaCas9 and an optimal Nrl-sg2 into the mouse retina. Excitingly, in vivo inactivation of Nrl improved photoreceptor cell survival and rescued retinal function in treated Pde6a-deficient mice. Thus, we showed that a practical, gene-independent method, AAV-SaCas9-mediated Nrl inactivation, holds promise for future therapeutic applications in patients with RP.

摘要

视网膜色素变性(RP)是一组复杂的遗传性视网膜疾病,其特征是光感受器细胞进行性死亡并最终导致失明。编码环磷酸鸟苷特异性磷酸二酯酶的Pde6a是常染色体隐性RP(RP43)的关键致病基因;目前尚无针对这种形式RP的有效治疗方法。紧凑的CRISPR/金黄色葡萄球菌Cas9(CRISPR/SaCas9)系统可以包装到单个腺相关病毒(AAV)中,有望简化有效的基因治疗。在这里,我们证明了一体化AAV-SaCas9介导的Nrl基因失活能够有效预防Pde6anmf363/nmf363突变的RP小鼠模型中的视网膜变性。我们在N2a细胞中筛选了能够有效编辑小鼠Nrl基因的单向导RNA,然后通过使用单个AAV将SaCas9和最佳的Nrl-sg2共递送到小鼠视网膜中实现了有效的基因编辑。令人兴奋的是,Nrl的体内失活改善了经治疗的Pde6a缺陷小鼠的光感受器细胞存活并挽救了视网膜功能。因此,我们表明一种实用的、不依赖基因的方法,即AAV-SaCas9介导的Nrl失活,有望在RP患者的未来治疗应用中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edcf/11665581/235b6ea2f546/jciinsight-9-178159-g232.jpg

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