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miR-210-3p 在年龄相关性白内障患者房水中的表达及其对过氧化氢诱导的人晶状体上皮细胞损伤的影响。

Expression of miR-210-3p in the aqueous humor of patients with age-related cataracts and its effect on human lens epithelial cell injury induced by hydrogen peroxide.

机构信息

Ophthalmology department, Jinhua Polytechnic, Jinhua, Zhejiang, 321000, China.

Cataract specialist, Jinhua Eye Hospital, Jinhua, Zhejiang, 321000, China.

出版信息

Arq Bras Oftalmol. 2023 Apr 17;87(5):e20220274. doi: 10.5935/0004-2749.2022-0274. eCollection 2023.


DOI:10.5935/0004-2749.2022-0274
PMID:39298734
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11627096/
Abstract

PURPOSE: The regulatory effect of microRNA on diseases has been confirmed. This study aimed to evaluate the expression of microRNA-210-3p in age-related cataracts and assess the effect of abnormal miR-210-3p expressions on H2O2-induced SAR01/04 cells. METHODS: Reverse-transcription quantitative polymerase chain reaction method was performed to assess the levels of miR-210-3p in aqueous humor samples. Receiver operating characteristic analysis was employed to assess the discrimination ability of miR-210-3p between patients with age-related cataracts and healthy people, and Pearson correlation analysis was used to identify the correlation between miR-210-3p and oxidative stress indices such as superoxide dismutase, glutathione peroxidase, malonaldehyde. Cell counting kit-8 assay and Transwell assay were used to estimate the biological function of H2O2-induced age-related cataract cell model. The levels of oxidative stress indices such as superoxide dismutase, glutathione peroxidase, and malonaldehyde were measured to evaluate the degree of oxidative stress damage in the age-related cataract cell model. The relationship between miR-210-3p and its target gene was verified by luciferase reporter gene analysis. RESULTS: The miR-210-3p expression was elevated in the aqueous humor of patients with age-related cataracts. A high miR-210-3p expression showed a high diagnostic value for age-related cataracts and was significantly associated with the level of oxidative stress markers in patients with age-related cataracts. The inhibition of miR-210-3p can reverse oxidative stress stimulation and adverse effects on H2O2-induced cell function. CONCLUSIONS: The results suggested that miR-210-3p could promote cell viability, cell migration, and oxidative stress by targeting autophagy-related gene 7 in in vitro age-related cataract cell model.

摘要

目的:已经证实 microRNA 对疾病具有调节作用。本研究旨在评估 microRNA-210-3p 在年龄相关性白内障中的表达,并评估异常 miR-210-3p 表达对 H2O2 诱导的 SAR01/04 细胞的影响。

方法:采用逆转录定量聚合酶链反应方法评估房水中 miR-210-3p 的水平。采用受试者工作特征分析评估 miR-210-3p 在年龄相关性白内障患者与健康人群之间的区分能力,并采用 Pearson 相关分析鉴定 miR-210-3p 与超氧化物歧化酶、谷胱甘肽过氧化物酶、丙二醛等氧化应激指标的相关性。细胞计数试剂盒-8 检测和 Transwell 检测用于评估 H2O2 诱导的年龄相关性白内障细胞模型的生物学功能。测量超氧化物歧化酶、谷胱甘肽过氧化物酶和丙二醛等氧化应激指标的水平,以评估年龄相关性白内障细胞模型的氧化应激损伤程度。通过荧光素酶报告基因分析验证 miR-210-3p 与其靶基因的关系。

结果:年龄相关性白内障患者房水中 miR-210-3p 表达升高。高 miR-210-3p 表达对年龄相关性白内障具有较高的诊断价值,与年龄相关性白内障患者的氧化应激标志物水平显著相关。抑制 miR-210-3p 可逆转氧化应激刺激和对 H2O2 诱导的细胞功能的不良影响。

结论:结果表明,miR-210-3p 可通过靶向自噬相关基因 7 促进体外年龄相关性白内障细胞模型中的细胞活力、细胞迁移和氧化应激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de3/11627096/e20dd363d57b/abo-87-05-e2022-0274-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de3/11627096/d970d70d073f/abo-87-05-e2022-0274-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de3/11627096/e4b63e211684/abo-87-05-e2022-0274-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de3/11627096/bde484bd6250/abo-87-05-e2022-0274-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de3/11627096/e20dd363d57b/abo-87-05-e2022-0274-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de3/11627096/d970d70d073f/abo-87-05-e2022-0274-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de3/11627096/e4b63e211684/abo-87-05-e2022-0274-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de3/11627096/bde484bd6250/abo-87-05-e2022-0274-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de3/11627096/e20dd363d57b/abo-87-05-e2022-0274-g04.jpg

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[1]
Expression of miR-210-3p in the aqueous humor of patients with age-related cataracts and its effect on human lens epithelial cell injury induced by hydrogen peroxide.

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[6]
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[7]
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引用本文的文献

[1]
miR-24-3p mediates Keap1/Nrf2 axis to promote autophagy and thereby inhibit lens epithelial cell early senescence.

Int Ophthalmol. 2025-8-9

[2]
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Int J Ophthalmol. 2024-5-18

本文引用的文献

[1]
Role of long noncoding RNA KCNQ1 overlapping transcript 1/microRNA-124-3p/BCL-2-like 11 axis in hydrogen peroxide (HO)-stimulated human lens epithelial cells.

Bioengineered. 2022-3

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A Network Pharmacology Study on the Molecular Mechanism of Protocatechualdehyde in the Treatment of Diabetic Cataract.

Drug Des Devel Ther. 2021

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Hsa_circ_0004058 inhibits apoptosis of SRA01/04 cells by promoting autophagy via miR-186/ATG7 axis.

Exp Eye Res. 2021-10

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EMT Participates in the Regulation of Exosomes Secretion and Function in Esophageal Cancer Cells.

Technol Cancer Res Treat. 2021

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Epigallocatechin-3-Gallate Alleviates High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease via Inhibition of Apoptosis and Promotion of Autophagy through the ROS/MAPK Signaling Pathway.

Oxid Med Cell Longev. 2021

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FXII regulates the formation of deep vein thrombosis via the PI3K/AKT signaling pathway in mice.

Int J Mol Med. 2021-5

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Long non-coding RNA KCNQ1OT1 promotes hydrogen peroxide-induced lens epithelial cell apoptosis and oxidative stress by regulating miR-223-3p/BCL2L2 axis.

Exp Eye Res. 2021-5

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