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miR-132-3p 在 CD4 T 细胞中下调,与狼疮患者的疾病表现相关。

miR-132-3p downregulates in CD4 T cells and is associated with disease manifestations in patients with lupus.

机构信息

Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.

出版信息

J Int Med Res. 2024 Oct;52(10):3000605241286762. doi: 10.1177/03000605241286762.

Abstract

OBJECTIVE

This study aimed to evaluate the expression status of miR-132-3p in CD4 T cells in patients with systemic lupus erythematosus (SLE) and explore its potential role in SLE development.

METHODS

The study included 60 patients with SLE and 30 healthy controls. miR-132-3p expression in CD4 T cells was detected by real-time quantitative reverse transcription polymerase chain. Bioinformatics analyses were employed to predict target genes and explore the potential role of miR-132-3p. The associations between miR-132-3p levels and SLE Disease Activity Index (SLEDAI) score, as well as laboratory characteristics, were analyzed.

RESULTS

miR-132-3p levels in CD4 T cells were significantly higher in patients with SLE compared with healthy controls. Bioinformatics analysis identified as a potential target gene of miR-132-3p, with a particular emphasis on the FOXO signaling pathway. miR-132-3p up-regulation in CD4 T cells was associated with high SLEDAI score, high anti-double-stranded DNA levels, low C3 and C4 levels, positive anti-ribosomal P, and high 24-hour urinary protein levels in patients with SLE.

CONCLUSIONS

miR-132-3p may contribute to CD4 T cell dysregulation during SLE by targeting and could potentially be used to assess disease severity.

摘要

目的

本研究旨在评估系统性红斑狼疮(SLE)患者 CD4 T 细胞中 miR-132-3p 的表达状态,并探讨其在 SLE 发病机制中的潜在作用。

方法

本研究纳入了 60 例 SLE 患者和 30 名健康对照者。采用实时定量逆转录聚合酶链反应检测 CD4 T 细胞中 miR-132-3p 的表达。通过生物信息学分析预测靶基因,并探讨 miR-132-3p 的潜在作用。分析 miR-132-3p 水平与 SLE 疾病活动指数(SLEDAI)评分以及实验室特征的相关性。

结果

SLE 患者 CD4 T 细胞中 miR-132-3p 水平明显高于健康对照组。生物信息学分析鉴定 为 miR-132-3p 的潜在靶基因,特别强调 FOXO 信号通路。SLE 患者 CD4 T 细胞中 miR-132-3p 的上调与 SLEDAI 评分高、抗双链 DNA 水平高、C3 和 C4 水平低、抗核糖体 P 阳性和 24 小时尿蛋白水平高相关。

结论

miR-132-3p 可能通过靶向 导致 CD4 T 细胞失调,从而参与 SLE 的发病机制,并可能用于评估疾病严重程度。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5723/11494630/07ade5adf5cc/10.1177_03000605241286762-fig1.jpg

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