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间充质干细胞来源的外泌体携带miR-125a-5p通过调节内质网应激来改善糖尿病角膜病变。

Mesenchymal stem cell-derived exosomes carry miR-125a-5p to improve diabetic keratopathy by regulating endoplasmic reticulum stress.

作者信息

Li Weina, He Shiping, Lin Chaoqun, Yang Sheng, Zhang Wenbin

机构信息

Ophthalmology Department, Nanxishan Hospital of Guangxi Zhuang Autonomous Region (The second Hospital of Guangxi Zhuang Autonomous Region), Guilin, Guangxi 541000, China; Ophthalmology Department, The Second Affiliated Hospital of Guangxi University of Science and Technology, Liuzhou, Guangxi 545005, China.

Glaucoma and Cataract Department, Liuzhou Aier Ophthalmology Hospital, Liuzhou, Guangxi 545005, China.

出版信息

Tissue Cell. 2025 Apr;93:102669. doi: 10.1016/j.tice.2024.102669. Epub 2024 Dec 5.

Abstract

BACKGROUND

Diabetic keratopathy is a prevalent but sometimes ignored visual condition in diabetic patients, which significantly affects patients with diabetes mellitus (DM) in terms of their visual acuity. Exosomes regulate diabetes-related conditions like diabetic keratopathy (DK) by secreting their components into the body.

OBJECTIVE

Aim to investigate the effect and mechanism of mesenchymal stem cell (MSC)-derived exosome miR-125a-5p on DK.

METHODS

Transmission electron microscopy, along with nanoparticle tracking analysis, was used to determine the morphology and size of exosomes. To evaluate cell viability, proliferation, and migration, Western blotting and RT-qPCR methods were used. CCK-8, cell cloning, and scratch assays were used to measure protein levels and mRNA expression.

RESULTS

High glucose treatment of corneal epithelial cells weakened cell viability, proliferation and migration, and the level of miR-125a-5p was significantly reduced. It has been proposed that elevated levels of miR-125a-5p could enhance cell viability, proliferation, and migration, can inhibit endoplasmic reticulum stress induced by high glucose, which is the same as the effect of endoplasmic reticulum stress inhibitors.

CONCLUSION

Mouse bone marrow MSC-derived exosome miR-125a-5p repairs corneal epithelial cell viability and proliferation as well as migration ability to improve DK by inhibiting high glucose-induced endoplasmic reticulum stress.

摘要

背景

糖尿病角膜病变是糖尿病患者中一种常见但有时被忽视的视力问题,在视力方面对糖尿病患者有显著影响。外泌体通过将其成分分泌到体内来调节糖尿病相关病症,如糖尿病角膜病变(DK)。

目的

旨在研究间充质干细胞(MSC)来源的外泌体miR-125a-5p对DK的作用及机制。

方法

采用透射电子显微镜和纳米颗粒跟踪分析来确定外泌体的形态和大小。使用蛋白质印迹法和RT-qPCR方法评估细胞活力、增殖和迁移。采用CCK-8、细胞克隆和划痕试验来测量蛋白质水平和mRNA表达。

结果

高糖处理角膜上皮细胞会削弱细胞活力、增殖和迁移,且miR-125a-5p水平显著降低。研究表明,miR-125a-5p水平升高可增强细胞活力、增殖和迁移,可抑制高糖诱导的内质网应激,这与内质网应激抑制剂的作用相同。

结论

小鼠骨髓MSC来源的外泌体miR-125a-5p通过抑制高糖诱导的内质网应激来修复角膜上皮细胞活力、增殖以及迁移能力,从而改善DK。

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