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长链非编码 RNA(lncRNA)SNHG5 在难治性糖尿病性黄斑水肿患者中的表达及其调控机制。

Expression of Long Non-Coding RNA (lncRNA) SNHG5 in Patients with Refractory Diabetic Macular Edema and Its Regulatory Mechanism.

机构信息

Department of Retinal and Vitreous Diseases, Aier Eye Hospital of Wuhan University, Wuhan, Hubei, China (mainland).

Department of Ophthalmic Imaging, Aier Eye Hospital of Wuhan University, Wuhan, Hubei, China (mainland).

出版信息

Med Sci Monit. 2022 Jan 10;28:e932996. doi: 10.12659/MSM.932996.

DOI:10.12659/MSM.932996
PMID:35001073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8762959/
Abstract

BACKGROUND The aim of this study was to assess use of lncRNAs as biomarkers in serum and aqueous humor of patients with diabetic macular edema (DME). MATERIAL AND METHODS Optical coherence tomography and fundus photography were used to analyze the retinal features of the patients. RT-qPCR was used to analyze the differential expression of lncRNA snhg5 in patients who have idiopathic macular hole (MH), DME, or refractory DME. The relationship between SNHG5 and the clinical characteristics of the patients was analyzed. The effect of SNHG5 on the hyperplasia and apoptosis of human retino-microvascular endothelial cells (HRMECs) and its mechanism were analyzed in vitro. RESULTS Patients with idiopathic MH developed retinal nerve epithelium rupture and retinal fundus thickening, and patients with DME or refractory DME showed significant macular edema with hemorrhaging. The refractory DME patients improved after treatment but still showed significant macular edema and multiple laser scarring. SNHG5 expression was not only low in the atrial fluid and plasma in DME patients, but also lower in the refractory DME group compared to the idiopathic MH patients. SNHG5 expression in the aqueous humor and plasma was negatively correlated with disease duration, body mass index, and levels of fasting blood glucose, glycated hemoglobin, proteinuria, and glycosuria. In the in vitro experiments, SNHG5 expression was significantly downregulated in high glucose-induced HMECs. After SNHG5 overexpression, cell proliferation, angiogenesis, and VEGF-A protein levels were distinctly downregulated. CONCLUSIONS SNHG5 correlates with the development of DME and is a potential target for therapy.

摘要

背景

本研究旨在评估 lncRNA 作为糖尿病黄斑水肿(DME)患者血清和房水中生物标志物的应用。

材料与方法

应用光学相干断层扫描和眼底照相分析患者的视网膜特征。应用 RT-qPCR 分析特发性黄斑裂孔(MH)、DME 或难治性 DME 患者中 lncRNA snhg5 的差异表达。分析 SNHG5 与患者临床特征的关系。体外分析 SNHG5 对人视网膜微血管内皮细胞(HRMEC)增生和凋亡的影响及其机制。

结果

特发性 MH 患者发生视网膜神经上皮破裂和眼底增厚,DME 或难治性 DME 患者表现为明显黄斑水肿伴出血。难治性 DME 患者经治疗后好转,但仍存在明显的黄斑水肿和多处激光瘢痕。DME 患者房水和血浆中的 SNHG5 表达不仅降低,而且与特发性 MH 患者相比,难治性 DME 组的 SNHG5 表达更低。房水和血浆中的 SNHG5 表达与疾病持续时间、体重指数以及空腹血糖、糖化血红蛋白、蛋白尿和糖尿水平呈负相关。在体外实验中,高糖诱导的 HMEC 中 SNHG5 表达明显下调。过表达 SNHG5 后,细胞增殖、血管生成和 VEGF-A 蛋白水平明显下调。

结论

SNHG5 与 DME 的发生发展相关,是治疗的潜在靶点。

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