{"title":"miR-132-3p 下调 CD4+ T 细胞中的 FOXO1,并与狼疮患者的疾病表现相关。","authors":"Haihong Qin, Sunyi Chen, Xiao Liu, Jun Liang, Hao Wu, Xiaohua Zhu","doi":"10.1177/03000605241286762","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to evaluate the expression status of miR-132-3p in CD4<sup>+</sup> T cells in patients with systemic lupus erythematosus (SLE) and explore its potential role in SLE development.</p><p><strong>Methods: </strong>The study included 60 patients with SLE and 30 healthy controls. miR-132-3p expression in CD4<sup>+</sup> 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.</p><p><strong>Results: </strong>miR-132-3p levels in CD4<sup>+</sup> T cells were significantly higher in patients with SLE compared with healthy controls. Bioinformatics analysis identified <i>FOXO1</i> 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<sup>+</sup> 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.</p><p><strong>Conclusions: </strong>miR-132-3p may contribute to CD4<sup>+</sup> T cell dysregulation during SLE by targeting <i>FOXO1</i> and could potentially be used to assess disease severity.</p>","PeriodicalId":16129,"journal":{"name":"Journal of International Medical Research","volume":null,"pages":null},"PeriodicalIF":1.4000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11494630/pdf/","citationCount":"0","resultStr":"{\"title\":\"miR-132-3p downregulates <i>FOXO1</i> in CD4<sup><b>+</b></sup> T cells and is associated with disease manifestations in patients with lupus.\",\"authors\":\"Haihong Qin, Sunyi Chen, Xiao Liu, Jun Liang, Hao Wu, Xiaohua Zhu\",\"doi\":\"10.1177/03000605241286762\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>This study aimed to evaluate the expression status of miR-132-3p in CD4<sup>+</sup> T cells in patients with systemic lupus erythematosus (SLE) and explore its potential role in SLE development.</p><p><strong>Methods: </strong>The study included 60 patients with SLE and 30 healthy controls. miR-132-3p expression in CD4<sup>+</sup> 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.</p><p><strong>Results: </strong>miR-132-3p levels in CD4<sup>+</sup> T cells were significantly higher in patients with SLE compared with healthy controls. Bioinformatics analysis identified <i>FOXO1</i> 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<sup>+</sup> 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.</p><p><strong>Conclusions: </strong>miR-132-3p may contribute to CD4<sup>+</sup> T cell dysregulation during SLE by targeting <i>FOXO1</i> and could potentially be used to assess disease severity.</p>\",\"PeriodicalId\":16129,\"journal\":{\"name\":\"Journal of International Medical Research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.4000,\"publicationDate\":\"2024-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11494630/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of International Medical Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1177/03000605241286762\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of International Medical Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/03000605241286762","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0
摘要
研究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 的表达状况,并探讨其在系统性红斑狼疮发展过程中的潜在作用:研究纳入了60名系统性红斑狼疮患者和30名健康对照者,采用实时定量反转录聚合酶链法检测CD4+ T细胞中miR-132-3p的表达。研究人员利用生物信息学分析预测靶基因,并探索 miR-132-3p 的潜在作用。结果发现:与健康对照组相比,系统性红斑狼疮患者 CD4+ T 细胞中的 miR-132-3p 水平明显更高。miR-132-3p在CD4+ T细胞中的上调与系统性红斑狼疮患者的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小时尿蛋白水平高有关。结论:miR-132-3p 可通过靶向 FOXO1 导致系统性红斑狼疮期间 CD4+ T 细胞失调,并有可能用于评估疾病的严重程度。
miR-132-3p downregulates FOXO1 in CD4+ T cells and is associated with disease manifestations in patients with lupus.
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 FOXO1 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 FOXO1 and could potentially be used to assess disease severity.
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