State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, China.
State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, China.
Exp Eye Res. 2023 Aug;233:109551. doi: 10.1016/j.exer.2023.109551. Epub 2023 Jun 23.
The study aimed to investigate the role of microRNA (miR)-124-3p in retinal angiogenesis in a mouse model. An intravitreal injection of miR-124-3p antagomir was used to knockdown the expression of miR-124-3p in the mouse retina at postnatal day (P)3. Immunofluorescent staining of both retinal frozen sections and whole retina were used to observe retinal vascular development in the P6, P9 and P12 mice, as well as the changes in retinal ganglion cells, astrocytes, Müller cells and microglia. Whole retinal RNA extracted from P9 mice was used for transcriptome sequencing. Following gene set enrichment analysis, the enriched genes caused by miR-124-3p inhibition were analyzed by immunofluorescent staining and western blot. Results indicated that deep vascular development was significantly inhibited by the activation of M1 phenotype microglia. Moreover, there were no notable effects on superficial retinal vascular development, the retinal ganglion cells, astrocytes, and Müller cells. The expression of the Stat1/Irf9/Eif2ak2/Ripk1 axis in the miR-124-3p knockdown group was significantly increased. The microglia penetrated deep into the retina and the activation of Ripk1(+) microglia significantly increased, which was accompanied by an increased level of apoptosis to inhibit the deep vascular sprout. Downregulation of miR-124-3p during the early retinal development can suppress the development of the deep retinal blood vessels by enhancing the expression level of the Stat1/Irf9/Eif2ak2/Ripk1 axis and inducing the cell apoptosis of the activation of Ripk1(+) microglia.
本研究旨在探讨 microRNA (miR)-124-3p 在小鼠模型视网膜血管生成中的作用。在出生后第 3 天(P3),通过玻璃体内注射 miR-124-3p 拮抗剂来敲低小鼠视网膜中 miR-124-3p 的表达。使用视网膜冷冻切片和全视网膜免疫荧光染色来观察 P6、P9 和 P12 小鼠的视网膜血管发育情况,以及视网膜神经节细胞、星形胶质细胞、Müller 细胞和小胶质细胞的变化。从 P9 小鼠的全视网膜提取 RNA 进行转录组测序。在进行基因集富集分析后,通过免疫荧光染色和 Western blot 分析 miR-124-3p 抑制引起的富集基因。结果表明,M1 表型小胶质细胞的激活显著抑制了深层血管的发育。此外,对浅层视网膜血管发育、视网膜神经节细胞、星形胶质细胞和 Müller 细胞没有明显影响。miR-124-3p 敲低组中 Stat1/Irf9/Eif2ak2/Ripk1 轴的表达显著增加。小胶质细胞深入视网膜,Ripk1(+)小胶质细胞的激活显著增加,伴随着凋亡水平的增加,以抑制深层血管芽的生长。在早期视网膜发育过程中下调 miR-124-3p 可以通过增强 Stat1/Irf9/Eif2ak2/Ripk1 轴的表达水平并诱导 Ripk1(+)小胶质细胞的细胞凋亡来抑制深层视网膜血管的发育。