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Updated: Aug 1, 2026
Experimental Models for Study of Retinal Pigment Epithelial Physiology and Pathophysiology
Published on: November 6, 2010
MiR-6837-3p protected retinal epithelial cells from oxidative stress by targeting E2F6
Xin Zhao1, Xinru Chen1, Xiangyang Xin2
1Department of Ophthalmology, Baogang Hospital of Inner Mongolia, Baotou, 014010, Inner Mongolia, China.
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.
