Yang Jing, Yang Kun, Meng Xuxia, Liu Penghui, Fu Yudong, Wang Yibo
Ophthalmology, Affiliated Hospital of Qingdao University, Qingdao, 266500, Shandong Province, People's Republic of China.
Central Laboratory, Affiliated Hospital of Qingdao University, Qingdao, 266500, Shandong Province, People's Republic of China.
J Inflamm Res. 2021 Apr 20;14:1563-1573. doi: 10.2147/JIR.S299010. eCollection 2021.
The lncRNA small nucleolar RNA host gene 1 (SNHG1) is a cerebral infarction-associated gene, its biological role and mechanism in diabetic retinopathy remain to be illuminated. The present study was designed to investigate the role of SNHG1 in high glucose induced human retinal pigment epithelial cells (ARPE-19).
ARPE-19 cells were cultured and exposed to 60 mM high glucose for 48h, and 5.5mM glucose-exposed ARPE-19 cells were used as the control. The levels of the epithelial-mesenchymal transition (EMT) markers E-cadherin, ZO-1, vimentin and α-SMA were measured, and the Cell inflammatory response was evaluated by detecting IL-6 and IL-1β levels. Then, cell migration, proliferation and apoptosis were detected. The expression of the lncRNA SNHG1 in ARPE-19 cells was detected by quantitative real-time PCR. SNHG1 was knocked down by small interfering RNA (siRNA) transfection. The effects of SNHG1 inhibition on inflammation, EMT, migration, proliferation and apoptosis were observed.
The results showed that the expression of SNHG1 was significantly increased in ARPE-19 cells exposed to high glucose. Silencing SNHG1 reduced the expression of vimentin, α-SMA, and the expression of inflammatory chemokines IL-6 and IL-1β, inhibited migration and proliferation, elevated the expression of E-cadherin and ZO-1, and promoted apoptosis in ARPE-19 cells.
The lncRNA SNHG1 is involved in hyperglycemia-induced EMT and the inflammatory response of ARPE-19 cells and provides a new understanding of the pathogenesis of DR.
长链非编码RNA小核仁RNA宿主基因1（SNHG1）是一种与脑梗死相关的基因，其在糖尿病视网膜病变中的生物学作用及机制尚待阐明。本研究旨在探讨SNHG1在高糖诱导的人视网膜色素上皮细胞（ARPE-19）中的作用。
培养ARPE-19细胞并将其暴露于60 mM高糖环境中48小时，将暴露于5.5 mM葡萄糖的ARPE-19细胞作为对照。检测上皮-间质转化（EMT）标志物E-钙黏蛋白、紧密连接蛋白1（ZO-1）、波形蛋白和α-平滑肌肌动蛋白（α-SMA）的水平，并通过检测白细胞介素-6（IL-6）和白细胞介素-1β（IL-1β）水平评估细胞炎症反应。然后，检测细胞迁移、增殖和凋亡情况。通过定量实时PCR检测ARPE-19细胞中lncRNA SNHG1的表达。通过小干扰RNA（siRNA）转染敲低SNHG1。观察SNHG1抑制对炎症、EMT、迁移、增殖和凋亡的影响。
结果显示，暴露于高糖的ARPE-19细胞中SNHG1的表达显著增加。沉默SNHG1可降低波形蛋白、α-SMA的表达以及炎症趋化因子IL-6和IL-1β的表达，抑制迁移和增殖，提高E-钙黏蛋白和ZO-1的表达，并促进ARPE-19细胞凋亡。
lncRNA SNHG1参与高血糖诱导的ARPE-19细胞EMT和炎症反应，为糖尿病视网膜病变的发病机制提供了新的认识。
