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微小RNA-185-5p通过靶向趋化因子受体4参与调控视网膜微血管内皮细胞的异常增殖。

MiR-185-5p is Involved in Regulating the Abnormal Proliferation of Retinal Microvascular Endothelial Cells via Targeting CXCR4.

作者信息

Wen Xiaoxia, Tang Yunxia, Guo Hongjian

机构信息

Department of Ophthalmology, The People's Hospital of Kaizhou District, Chongqing, China.

Chongqing Kaizhou Aier Sunshine Eye Hospital, Chongqing, China.

出版信息

Curr Eye Res. 2025 Mar;50(3):334-343. doi: 10.1080/02713683.2024.2430224. Epub 2024 Nov 25.

Abstract

PURPOSE

This study aimed to explore the expression profile of miR-185-5p in proliferative DR (PDR), and further evaluate its diagnostic value and possible mechanism of miR-185-5p in PDR.

METHODS

The level of miR-185-5p was detected by qRT-PCR. The ROC curve was established to estimate the diagnostic ability of miR-185-5p. Transwell experiment and cell counting kit-8 (CCK-8) assays were conducted to assess the effect of miR-185-5p on the migration and proliferation of human retinal endothelial cells (HRECs) induced by high glucose. Enzyme linked immunosorbent assay (ELISA) was used to detect the concentrations of inflammatory factors. The luciferase reporter gene experiment was used to prove the interaction between miR-185-5p and CXCR4.

RESULTS

Compared to the control group, the expression of miR-185-5p was significantly up-regulated in both the type 2 diabetes mellitus (T2DM) group and the PDR groups, with higher levels in the PDR group than in the T2DM group. The ROC curve reveals that serum miR-185-5p can distinguish PDR patients from T2DM patients. MiR-185-5p levels in HRECs increased significantly after high glucose induction. High glucose induction also promoted the migration, proliferation and inflammation response of HRECs. However, when the intracellular miR-185-5p level was down-regulated by miR-185-5p inhibitor transfection, these effects were inhibited. The luciferase reporter gene assay showed that miR-185-5p directly targets CXCR4.

CONCLUSION

The expression of miR-185-5p is out of balance in PDR and it may be involved in regulating the migration and proliferation of HRECs by regulating CXCR4.

摘要

目的

本研究旨在探讨miR - 185 - 5p在增殖性糖尿病视网膜病变(PDR)中的表达谱,并进一步评估其在PDR中的诊断价值及可能机制。

方法

采用qRT - PCR检测miR - 185 - 5p水平。建立ROC曲线以评估miR - 185 - 5p的诊断能力。进行Transwell实验和细胞计数试剂盒 - 8(CCK - 8)检测,以评估miR - 185 - 5p对高糖诱导的人视网膜内皮细胞(HRECs)迁移和增殖的影响。采用酶联免疫吸附测定(ELISA)检测炎症因子浓度。利用荧光素酶报告基因实验证明miR - 185 - 5p与CXCR4之间的相互作用。

结果

与对照组相比,2型糖尿病(T2DM)组和PDR组中miR - 185 - 5p的表达均显著上调,PDR组水平高于T2DM组。ROC曲线显示血清miR - 185 - 5p可区分PDR患者与T2DM患者。高糖诱导后HRECs中miR - 185 - 5p水平显著升高。高糖诱导还促进了HRECs的迁移、增殖和炎症反应。然而,当通过转染miR - 185 - 5p抑制剂下调细胞内miR - 185 - 5p水平时,这些作用受到抑制。荧光素酶报告基因检测表明miR - 185 - 5p直接靶向CXCR4。

结论

miR - 185 - 5p在PDR中的表达失衡,可能通过调节CXCR4参与调控HRECs的迁移和增殖。

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