Retinopathy of prematurity (ROP) is a severe retinal dysfunction in prematurely born babies. The relationship between non-coding RNAs and retinopathy of prematurity (ROP) remain unclear. Microarray analysis of lncRNAs, miRNAs, and mRNAs was conducted in a mouse model of ROP. A competing endogenous RNA (ceRNA) network was constructed. The relationship among MALAT1, miR-124–3p, and Early growth response protein 1 (EGR1) was assessed in hypoxia-induced primary human umbilical vein endothelial cells (HUVECs) and ROP mouse model. In the study, we found 2252 lncRNAs, 1239 mRNAs, and 36 miRNAs were differentially regulated. ceRNA network consisting of 21 lncRNAs, 10 miRNAs, and 19 mRNAs was established. Of the most down-regulated miRNAs, miR-124–3p was selected for additional study. miR-124–3p ceased the migration and proliferation of primary HUVECs in hypoxic conditions, and directly suppressed EGR1. Additionally, MALAT1 directly sponged miR-124–3p. Knockdown of MALAT1 decreased EGR1 expression and inhibited the migration and proliferation of primary HUVECs in hypoxia. Furthermore, these changes were rescued by depletion of miR-124–3p. In vivo, intravitreal injection of miR-124–3p, shMALAT1 decreased EGR1 expression and markedly suppressed retinal neovascularization in OIR models. Intravitreal injection of shMALAT1 and miR-124–3p antagomir at the same time can promote retinal neovascularization, which reversed the suppression of retinal neovascularization functioned by shMALAT1. In conclusion, the expression profiles of lncRNAs and miRNAs and the ceRNA network in a mouse model of ROP may be indicative of the underlying mechanisms of retinal angiogenesis and neural activity. The MALAT1/miR-124–3p/EGR1 regulatory axis is partly responsible for retinal neovascularization, which may provide a novel theoretical basis for the pathogenesis of ROP.

早产儿视网膜病变（ROP）是早产儿的严重视网膜功能障碍。非编码 RNA 与早产儿视网膜病变 (ROP) 之间的关系仍不清楚。在 ROP 小鼠模型中进行 lncRNA、miRNA 和 mRNA 的微阵列分析。构建了竞争性内源 RNA (ceRNA) 网络。在缺氧诱导的原代人脐静脉内皮细胞 (HUVEC) 和 ROP 小鼠模型中评估了 MALAT1、miR-124–3p 和早期生长反应蛋白 1 (EGR1) 之间的关系。在研究中，我们发现 2252 个 lncRNA、1239 个 mRNA 和 36 个 miRNA 受到差异调节。建立了由21个lncRNA、10个miRNA和19个mRNA组成的ceRNA网络。在下调最多的 miRNA 中，选择 miR-124–3p 进行进一步研究。 miR-124-3p 在缺氧条件下停止原代 HUVEC 的迁移和增殖，并直接抑制 EGR1。此外，MALAT1 直接海绵 miR-124–3p。 MALAT1 的敲低降低了 EGR1 的表达，并抑制了原代 HUVEC 在缺氧条件下的迁移和增殖。此外，这些变化可以通过 miR-124-3p 的耗竭来挽救。在体内，玻璃体内注射 miR-124–3p、shMALAT1 可降低 OIR 模型中 EGR1 的表达并显着抑制视网膜新生血管形成。玻璃体内同时注射shMALAT1和miR-124-3p antagomir可以促进视网膜新生血管形成，从而逆转了shMALAT1对视网膜新生血管形成的抑制作用。总之，ROP 小鼠模型中 lncRNA 和 miRNA 以及 ceRNA 网络的表达谱可能表明视网膜血管生成和神经活动的潜在机制。 MALAT1/miR-124–3p/EGR1调节轴部分负责视网膜新生血管形成，这可能为ROP的发病机制提供新的理论基础。