Qiu Gui-Zhen, Tian Wei, Fu Hai-Tao, Li Chao-Peng, Liu Ban
Department of Health, Linyi People's Hospital, Shandong University, Shandong, China.
Department of Nursing, Linyi Oncosurgical Hospital, Shandong, China.
Biochem Biophys Res Commun. 2016 Feb 26;471(1):135-41. doi: 10.1016/j.bbrc.2016.01.164. Epub 2016 Feb 1.
Microvascular dysfunction is an important characteristic of diabetic retinopathy. Long non-coding RNAs (lncRNAs) play important roles in diverse biological processes. In this study, we investigated the role of lncRNA-MEG3 in diabetes-related microvascular dysfunction. We show that MEG3 expression level is significantly down-regulated in the retinas of STZ-induced diabetic mice, and endothelial cells upon high glucose and oxidative stress. MEG3 knockdown aggravates retinal vessel dysfunction in vivo, as shown by serious capillary degeneration, and increased microvascular leakage and inflammation. MEG3 knockdown also regulates retinal endothelial cell proliferation, migration, and tube formation in vitro. The role of MEG3 in endothelial cell function is mainly mediated by the activation of PI3k/Akt signaling. MEG3 up-regulation may serve as a therapeutic strategy for treating diabetes-related microvascular complications.
微血管功能障碍是糖尿病视网膜病变的一个重要特征。长链非编码RNA(lncRNAs)在多种生物学过程中发挥重要作用。在本研究中,我们调查了lncRNA-MEG3在糖尿病相关微血管功能障碍中的作用。我们发现,在链脲佐菌素诱导的糖尿病小鼠视网膜以及高糖和氧化应激条件下的内皮细胞中,MEG3表达水平显著下调。MEG3基因敲低会加重体内视网膜血管功能障碍,表现为严重的毛细血管变性、微血管渗漏增加和炎症。MEG3基因敲低还会在体外调节视网膜内皮细胞的增殖、迁移和管腔形成。MEG3在内皮细胞功能中的作用主要通过PI3k/Akt信号通路的激活来介导。上调MEG3可能是治疗糖尿病相关微血管并发症的一种治疗策略。