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miR-455-3p表达降低通过调节视网膜内皮细胞增殖和凋亡促进糖尿病视网膜病变进展。

Decreased miR-455-3p promotes diabetic retinopathy progression via modulating retinal endothelial proliferation and apoptosis.

作者信息

Jiang Weipeng, Xu Shouyan, Lu Shanshan, Dong Ailing, Jiang Neng

机构信息

Department of Ophthalmology, Taizhou First People's Hospital, No. 218, Hengjie Road, Huangyan District, Taizhou City, 318020, Zhejiang Province, China.

Department of Ophthalmology, Huangyan District Maternal and Child Health Hospital, Taizhou, 318020, China.

出版信息

BMC Ophthalmol. 2025 Jul 1;25(1):367. doi: 10.1186/s12886-025-04179-5.

Abstract

BACKGROUND

Diabetic retinopathy (DR) is one of the common ocular complications of diabetes. Recent studies have also found that miR-455-3p is dysregulated in DR. However, its underlying mechanisms warrant further investigation.

OBJECTIVE

This study focused on the clinical value of miR-455-3p and its regulatory mechanisms in DR.

MATERIALS AND METHODS

This study recruited 130 patients with DR and 105 healthy individuals. HRMECs treated with high glucose were used to simulate DR conditions. The expression of miR-455-3p and Integrin beta 1() were assessed by qRT-PCR while the target relationship between them was validated via Dual-luciferase reporter assay. ROC curve was utilized for the diagnostic performance. CCK-8 and flow cytometry were employed for proliferation and apoptosis measurement while ELISA was used for inflammation.

RESULTS

Serum miR-455-3p was found to be distinctly downregulated in patients with DR. The expression of serum miR-455-3p was negatively associated with HbA1c levels in patients with DR. The miR-455-3p also exhibited strong diagnostic potential for distinguishing patients with DR from healthy individuals. In high glucose-induced HRMECs, miR-455-3p was significantly downregulated. miR-455-3p can target and negatively regulate , thereby inhibiting the proliferation and inflammation of HRMECs induced by high glucose and promoting cell apoptosis.

CONCLUSION

Decreased miR-455-3p promotes diabetic retinopathy progression via negative regulation on .

CLINICAL TRIAL NUMBER

Not applicable.

摘要

背景

糖尿病视网膜病变(DR)是糖尿病常见的眼部并发症之一。最近的研究还发现,miR-455-3p在DR中表达失调。然而,其潜在机制有待进一步研究。

目的

本研究聚焦于miR-455-3p在DR中的临床价值及其调控机制。

材料与方法

本研究招募了130例DR患者和105名健康个体。用高糖处理的人视网膜微血管内皮细胞(HRMECs)来模拟DR条件。通过qRT-PCR评估miR-455-3p和整合素β1(Integrin beta 1)的表达,同时通过双荧光素酶报告基因检测验证它们之间的靶向关系。利用ROC曲线评估诊断性能。采用CCK-8和流式细胞术检测细胞增殖和凋亡,ELISA检测炎症反应。

结果

发现DR患者血清miR-455-3p明显下调。DR患者血清miR-455-3p的表达与糖化血红蛋白(HbA1c)水平呈负相关。miR-455-3p在区分DR患者和健康个体方面也具有很强的诊断潜力。在高糖诱导的HRMECs中,miR-455-3p显著下调。miR-455-3p可以靶向并负向调节整合素β1,从而抑制高糖诱导的HRMECs的增殖和炎症反应,并促进细胞凋亡。

结论

miR-455-3p的降低通过对整合素β1的负向调节促进糖尿病视网膜病变的进展。

临床试验编号

不适用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83e6/12220737/dfcdda587b17/12886_2025_4179_Fig1_HTML.jpg

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