The impact of miR-26b on retinal pigment epithelium cells in rhegmatogenous retinal detachment model

被引:0
作者
Zhang, Ruifan [1 ,2 ,3 ]
Liu, Zhirong [2 ,3 ]
Chen, Bo [2 ,3 ]
Zhang, Junjun [1 ]
机构
[1] Sichuan Univ, Dept Ophthalmol, West China Hosp, 37 Guoxue Xiang, Chengdu, Sichuan, Peoples R China
[2] Sichuan Acad Med Sci, Dept Ophthalmol, Chengdu, Sichuan, Peoples R China
[3] Sichuan Prov Peoples Hosp, Chengdu, Sichuan, Peoples R China
关键词
MiR-26b; rhegmatogenous retinal detachment; retinal pigment epithelium; proliferation; invasion; MESENCHYMAL TRANSITION; OXIDATIVE STRESS; MICRORNA-26B; VITRECTOMY; MIGRATION; CANCER; REPAIR;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Rhegmatogenous retinal detachment (RRD) is a type of blind eye disease that seriously affects the physical and mental health. The early pathological changes are closely related to the migration of retinal pigment epithelium (RPE) cells to the vitreous body. It was showed miR-26b plays an important role in regulating lens epithelial cell growth and proliferation. However, the expression and role of miR-26b in RPE from RRD is still unclear. Rabbit RRD model was established. RPE cells were isolated and cultivated. MiR-26b inhibitor was transfected to RPE cells from model group. MiR-26b expression was tested by Real-time PCR. RPE cell proliferation was evaluated by MTT assay. Ki-67 and PCNA expressions were detected by Western blot. Caspase 3 activity was measured by the kit. RPE cell invasion was determined by Transwell assay. MiR-26b significantly increased in RPE cells from model group. It obviously promoted RPE cell proliferation and invasion, suppressed Caspase 3 activity, and upregulated Ki-67 and PCNA expression compared with control (P < 0.05). MiR-26b inhibitor transfection markedly restrained RPE cell proliferation and invasion, enhanced Caspase 3 activity, and inhibited Ki-67 and PCNA levels compared with model group (P < 0.05). MiR-26b expression was upregulated in RRD. Downregulation of miR-26b can postpone the occurrence and development of RRD through inhibiting Ki-67 and PCNA, regulating cell apoptosis, and restraining RPE cell proliferation and invasion.
引用
收藏
页码:8141 / 8147
页数:7
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