MiR-124 Promotes the Growth of Retinal Ganglion Cells Derived from Müller Cells

Cellular Physiology and Biochemistry

Ye He¹ 

关键词: Mü;    ller cells;    Stem cells;    Retinal ganglion cells;    Atoh7;    MiR-124;   

DOI  :  10.1159/000487292

学科分类：分子生物学，细胞生物学和基因

来源: S Karger AG

【 摘 要 】

Background/Aims Retinal Müller cells could be induced to differentiate into retinal ganglion cells (RGCs), but RGCs derived from Müller cells have defects in axon growth, leading to a defect in signal conduction. In this study we aimed to explore the role of miR-124 in axon growth of RGCs derived from Müller cells. Methods Müller cells were isolated from rat retina and induced to dedifferentiate into retinal stem cells. The stem cells were infected by PGC-FU-Atoh7-GFP lentivirus and then transfected with miR-124 or anti-miR-124, and the length of axon was compared. Furthermore, the cells were injected into the eyes of rat chronic ocular hypertension glaucoma model and axon growth in vivo was examined. The targeting of CoREST by miR-124 was detected by luciferase assay. Results In retinal stem cells, the length of axon was 1,792±64.54 µm in miR-124 group, 509±21.35 µm in control group, and only 87.9±9.24 µm in anti-miR-124 group. In rat model, miR-124 promoted axon growth of RGCs differentiated from retinal stem cells. Furthermore, we found that miR-124 negatively regulated CoREST via directly targeting the binding site in CoREST 3′ UTR. Conclusions We provide the first evidence that miR-124 regulates axon growth of RGCs derived from Müller cells, and miR-124 has translational potential for gene therapy of glaucoma.

【 授权许可】

CC BY-NC-ND