Zhu Yun-Xi, Yao Jin, Liu Chang, Hu Hai-Tao, Li Xiu-Miao, Ge Hui-Min, Zhou Yun-Fan, Shan Kun, Jiang Qin, Yan Biao
Eye Hospital, Nanjing Medical University, Nanjing, China; The Fourth School of Clinical Medicine, Nanjing Medical University, Nanjing, China.
The Fourth School of Clinical Medicine, Nanjing Medical University, Nanjing, China; Eye Institute, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Biochem Biophys Res Commun. 2018 Feb 19;496(4):1236-1242. doi: 10.1016/j.bbrc.2018.01.177. Epub 2018 Feb 1.
Excessive light exposure leads to retinal degeneration and accelerates the progression and severity of several ocular diseases, such as age-related macular degeneration (AMD) and retinitis pigmentosa. Long non-coding RNAs (LncRNAs) have emerged as important regulators of photoreceptor development and ocular diseases. In this study, we investigated the role of lncRNA-MEG3 in light-induced retinal degeneration. MEG3 expression was significantly up-regulated after light insult in vivo and in vitro. MEG3 silencing protected against light-induced retinal degeneration in vivo and light-induced photoreceptor cell apoptosis in vitro. Mechanistically, MEG3 regulated retinal photoreceptor cell function by acting as p53 decoy. MEG3 silencing decreased caspase 3/7 activity, up-regulated anti-apoptotic protein (Bcl-2) expression, and down-regulated pro-apoptotic protein (Bax) expression. Taken together, this study provides a promising method of MEG3 silencing for treating light-induced retinal degeneration.
过度光照会导致视网膜变性，并加速几种眼部疾病的进展和严重程度，如年龄相关性黄斑变性（AMD）和色素性视网膜炎。长链非编码RNA（LncRNAs）已成为光感受器发育和眼部疾病的重要调节因子。在本研究中，我们研究了lncRNA-MEG3在光诱导的视网膜变性中的作用。在体内和体外光损伤后，MEG3表达显著上调。MEG3沉默在体内可预防光诱导的视网膜变性，在体外可预防光诱导的光感受器细胞凋亡。机制上，MEG3通过充当p53诱饵来调节视网膜光感受器细胞功能。MEG3沉默降低了caspase 3/7活性，上调了抗凋亡蛋白（Bcl-2）的表达，并下调了促凋亡蛋白（Bax）的表达。综上所述，本研究为治疗光诱导的视网膜变性提供了一种有前景的MEG3沉默方法。
