Abstract：
Retinal ganglion cells (RGCs) apoptosis is a vital manifestation of retinal ischemia/reperfusion (I/R) injury, yet the underlying mechanisms are not well understood. The contribution of long noncoding RNAs (lncRNAs) to this cellular process is currently being explored. Based on a lncRNA chip assay, we aimed to investigate the role of lncRNA uc007nnj.1 in the pathological process of ischemia-induced RGCs apoptosis.
Hank\'s balanced salt solution containing 10 µM antimycin A and 2 µM calcium ionophore for 2 h to construct an ischemic model in RGCs, and elevation of intraocular pressure to 120 mm Hg for 1 h was used to construct a mouse model of retinal I/R injury.
In this study, lncRNA uc007nnj.1 was highly upregulated in response to I/R injury in RGCs and mouse retinas. In addition, lncRNA uc007nnj.1 knockdown reduced retinal neuronal cell apoptosis in vitro and in vivo and significantly improved retinal function.
Mechanistically, the results demonstrated that lncRNA uc007nnj.1 acts as ceRNA competitively binding miR-155-5p, thereby enhancing the expression levels of Tle4, thus aggravating ischemia-related apoptosis in RGCs.
Finally, our study identifies the lncRNA uc007nnj.1/miR-155-5p/Tle4 axis as a potential target for the prevention of I/R-induced retinal neuronal death.
Hank\'s balanced salt solution containing 10 µM antimycin A and 2 µM calcium ionophore for 2 h to construct an ischemic model in RGCs, and elevation of intraocular pressure to 120 mm Hg for 1 h was used to construct a mouse model of retinal I/R injury.
In this study, lncRNA uc007nnj.1 was highly upregulated in response to I/R injury in RGCs and mouse retinas. In addition, lncRNA uc007nnj.1 knockdown reduced retinal neuronal cell apoptosis in vitro and in vivo and significantly improved retinal function.
Mechanistically, the results demonstrated that lncRNA uc007nnj.1 acts as ceRNA competitively binding miR-155-5p, thereby enhancing the expression levels of Tle4, thus aggravating ischemia-related apoptosis in RGCs.
Finally, our study identifies the lncRNA uc007nnj.1/miR-155-5p/Tle4 axis as a potential target for the prevention of I/R-induced retinal neuronal death.
摘要：
背景：视网膜神经节细胞（RGCs）凋亡是视网膜缺血/再灌注（I/R）损伤的重要表现，然而，潜在的机制还没有得到很好的理解。目前正在探索长链非编码RNA（lncRNA）对该细胞过程的贡献。基于lncRNA芯片检测，我们旨在研究lncRNAuc007nnj.1在缺血诱导的RGCs凋亡的病理过程中的作用。
方法：汉克的平衡盐溶液含有10µM抗霉素A和2µM钙离子载体2h，在RGC中构建缺血模型，并将眼压升高至120mmHg1h，以构建小鼠视网膜I/R损伤模型。
结果：在这项研究中，lncRNAuc007nnj.1响应于RGC和小鼠视网膜中的I/R损伤而高度上调。此外,lncRNAuc007nnj.1敲除在体外和体内减少视网膜神经元细胞凋亡，并显着改善视网膜功能。
结论：机械上，结果表明，lncRNAuc007nnj.1作为CERNA竞争性结合miR-155-5p，从而增强Tle4的表达水平,从而加重RGCs中缺血相关的凋亡。
结论：最后，我们的研究将lncRNAuc007nnj.1/miR-155-5p/Tle4轴确定为预防I/R诱导的视网膜神经元死亡的潜在靶标。
方法：汉克的平衡盐溶液含有10µM抗霉素A和2µM钙离子载体2h，在RGC中构建缺血模型，并将眼压升高至120mmHg1h，以构建小鼠视网膜I/R损伤模型。
结果：在这项研究中，lncRNAuc007nnj.1响应于RGC和小鼠视网膜中的I/R损伤而高度上调。此外,lncRNAuc007nnj.1敲除在体外和体内减少视网膜神经元细胞凋亡，并显着改善视网膜功能。
结论：机械上，结果表明，lncRNAuc007nnj.1作为CERNA竞争性结合miR-155-5p，从而增强Tle4的表达水平,从而加重RGCs中缺血相关的凋亡。
结论：最后，我们的研究将lncRNAuc007nnj.1/miR-155-5p/Tle4轴确定为预防I/R诱导的视网膜神经元死亡的潜在靶标。
