DUSP23 is over‐expressed and linked to the expression of DNMTs in CD4+ T cells from systemic lupus erythematosus patients

E. Balada, L. Felip, J. Ordi‐Ros, M. Vilardell‐Tarrés
{"title":"DUSP23 is over‐expressed and linked to the expression of DNMTs in CD4+ T cells from systemic lupus erythematosus patients","authors":"E. Balada, L. Felip, J. Ordi‐Ros, M. Vilardell‐Tarrés","doi":"10.1111/cei.12883","DOIUrl":null,"url":null,"abstract":"We evaluated the transcriptional expression of dual‐specificity protein phosphatase 23 (DUSP23) in CD4+ T cells from 30 systemic lupus erythematosus (SLE) patients and 30 healthy controls. DUSP23 mRNA levels were considerably higher in the patient group: 1490 ± 1713 versus 294·1 ± 204·2. No association was found between DUSP23 mRNA expression and the presence of typical serological and clinical parameters associated with SLE. Meaningful statistical values were obtained in the patient group between the levels of DUSP23 and integrin subunit alpha L (ITGAL), perforin 1 (PRF1) and CD40L. Similarly, transcript levels of different DNA methylation‐related enzymes [DNA methylation‐related enzymes (DNMT1, DNMT3A, DNMT3B, MBD2, and MBD4)] were also correlated positively with the expression of DUSP23. In an attempt to counteract the hypomethylation status of the promoters of certain genes known to be over‐expressed in SLE, it is possible that DUSP23 acts as a negative regulatory mechanism which ultimately silences the transcription of these epigenetically regulated genes by triggering an increase in the expression of different DNMTs.","PeriodicalId":10179,"journal":{"name":"Clinical & Experimental Immunology","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2016-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical & Experimental Immunology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1111/cei.12883","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 9

Abstract

We evaluated the transcriptional expression of dual‐specificity protein phosphatase 23 (DUSP23) in CD4+ T cells from 30 systemic lupus erythematosus (SLE) patients and 30 healthy controls. DUSP23 mRNA levels were considerably higher in the patient group: 1490 ± 1713 versus 294·1 ± 204·2. No association was found between DUSP23 mRNA expression and the presence of typical serological and clinical parameters associated with SLE. Meaningful statistical values were obtained in the patient group between the levels of DUSP23 and integrin subunit alpha L (ITGAL), perforin 1 (PRF1) and CD40L. Similarly, transcript levels of different DNA methylation‐related enzymes [DNA methylation‐related enzymes (DNMT1, DNMT3A, DNMT3B, MBD2, and MBD4)] were also correlated positively with the expression of DUSP23. In an attempt to counteract the hypomethylation status of the promoters of certain genes known to be over‐expressed in SLE, it is possible that DUSP23 acts as a negative regulatory mechanism which ultimately silences the transcription of these epigenetically regulated genes by triggering an increase in the expression of different DNMTs.
DUSP23在系统性红斑狼疮患者的CD4+ T细胞中过表达并与dnmt的表达相关
我们评估了30例系统性红斑狼疮(SLE)患者和30例健康对照者的CD4+ T细胞中双特异性蛋白磷酸酶23 (DUSP23)的转录表达。患者组DUSP23 mRNA水平明显较高,分别为1490±1713和294·1±204·2。未发现DUSP23 mRNA表达与SLE相关的典型血清学和临床参数存在关联。患者组DUSP23与整合素亚单位α L (ITGAL)、穿孔素1 (PRF1)、CD40L水平比较,差异有统计学意义。同样,不同DNA甲基化相关酶[DNA甲基化相关酶(DNMT1、DNMT3A、DNMT3B、MBD2和MBD4)]的转录水平也与DUSP23的表达呈正相关。为了抵消已知在SLE中过度表达的某些基因启动子的低甲基化状态,DUSP23可能作为一种负调控机制,通过触发不同dnmt表达的增加,最终使这些表观遗传调控基因的转录沉默。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信