MiR-6837-3p protected retinal epithelial cells from oxidative stress by targeting E2F6.

IF 1.4 4区医学 Q3 OPHTHALMOLOGY

International Ophthalmology Pub Date : 2025-05-09 DOI:10.1007/s10792-025-03540-3

Xin Zhao, Xinru Chen, Xiangyang Xin

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引用次数: 0

Abstract

Aim: The mechanism of age-related macular degeneration (AMD) is a complex illness that is not fully understood. Therefore, the aim of this study was to investigate the expression patterns of miR-6837-3p in retinal epithelial cells.

Methods: H₂O₂ was used to treat ARPE-19 cells for 2, 4 and 6 h to mimic the in vivo environment of AMD. MiR inhibitors and mimics were used to inhibit or overexpress miR-6837-3p in H₂O₂-treated ARPE-19 cells, respectively. Then, CCK8 assay, flow cytometry, and wound healing assays were conducted to assess the effects of miR-6837-3p on the behaviors of ARPE-19 cells, including cell growth, apoptosis, cycle progression, and migration. Finally, microRNA database prediction and luciferase reporter assays were used to demonstrate that miR-6837-3p targets the downstream gene E2F6.

Results: H₂O₂ induced a decrease in cell viability and an increase in ROS levels in a time-dependent manner. Additionally, overexpression of miR-6837-3p increased cell viability and suppressed apoptosis in ARPE-19 cells treated with H₂O₂. Meanwhile, increased miR-6837-3p promoted cell cycle progression and cell migration of ARPE-19 cells. Finally, miR-6837-3p exerted anti-apoptosis and anti-oxidative stress effects by inhibiting the expression of E2F6 in ARPE-19 cells.

Conclusions: The MiR-6837-3p/E2F6 axis might be a target for the treatment of AMD to improve ARPE-19 cell function.

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MiR-6837-3p通过靶向E2F6保护视网膜上皮细胞免受氧化应激。

目的：老年性黄斑变性（AMD）的发病机制是一种尚未完全了解的复杂疾病。因此，本研究的目的是研究miR-6837-3p在视网膜上皮细胞中的表达模式。方法：用H2O2处理ARPE-19细胞2、4、6 h，模拟AMD的体内环境。MiR抑制剂和模拟物分别在h2o2处理的ARPE-19细胞中抑制或过表达MiR -6837-3p。然后，通过CCK8实验、流式细胞术和伤口愈合实验来评估miR-6837-3p对ARPE-19细胞行为的影响，包括细胞生长、凋亡、周期进展和迁移。最后，使用microRNA数据库预测和荧光素酶报告基因检测来证明miR-6837-3p靶向下游基因E2F6。结果：H2O2诱导细胞活力降低，ROS水平升高，且呈时间依赖性。此外，在过氧化氢处理的ARPE-19细胞中，过表达miR-6837-3p可提高细胞活力并抑制凋亡。同时，miR-6837-3p的升高促进了ARPE-19细胞的细胞周期进程和细胞迁移。最后，miR-6837-3p通过抑制ARPE-19细胞中E2F6的表达发挥抗凋亡和抗氧化应激作用。结论：MiR-6837-3p/E2F6轴可能是治疗AMD改善ARPE-19细胞功能的靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

International Ophthalmology OPHTHALMOLOGY-

CiteScore

3.20

自引率

0.00%

发文量

451

期刊介绍： International Ophthalmology provides the clinician with articles on all the relevant subspecialties of ophthalmology, with a broad international scope. The emphasis is on presentation of the latest clinical research in the field. In addition, the journal includes regular sections devoted to new developments in technologies, products, and techniques.