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细胞因子信号传导抑制因子3基因启动子异常甲基化变化与克罗恩病易感性的关联

Association of Aberrant Promoter Methylation Changes in the Suppressor of Cytokine Signaling 3 Gene with Susceptibility to Crohn's Disease.

作者信息

Sanati Golshid, Jafari Davood, Noruzinia Mehrdad, Ebrahimi Daryani Naser, Ahmadvand Mohammad, Teimourian Shahram, Rezaei Nima

机构信息

Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Department of Immunology, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.

出版信息

Avicenna J Med Biotechnol. 2022 Apr-Jun;14(2):165-169. doi: 10.18502/ajmb.v14i2.8887.

DOI:10.18502/ajmb.v14i2.8887
PMID:35633985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9077662/
Abstract

BACKGROUND

Growing evidence supports that changes in the methylation state of Inflammatory Bowel Disease (IBD)-associated genes could significantly alter levels of gene expression, potentially contributing to disease onset and progression. We supposed that alterations in DNA methylation status at promoter region within the suppressor of cytokine signaling 3 gene in intestinal tissues may be involved in the susceptibility to Crohn's Disease (CD).

METHODS

DNA methylation status in the promoter region of the human gene of intestinal tissues from 15 patients with CD and 15 age- and sex-matched healthy controls were profiled using the real-time Quantitative Multiplex Methylation Specific PCR (QM-MSP) assay.

RESULTS

Based on methylation assay data profiling, we found that patients with CD showed a higher degree of methylation of the gene promoter region than did the healthy controls (unmethylated DNA in CD healthy controls; 0.00048±0.0011 0.07±0.142, p<0.000).

CONCLUSION

The data presented here demonstrate that aberrant methylation of the CpG islands within promoter regions of gene in colonic mucosa of CD was associated with mucosal inflammatory status, providing insights into the involvement of methylation could contribute to the initiation of the inflammatory process and development of CD.

摘要

背景

越来越多的证据支持,炎症性肠病(IBD)相关基因甲基化状态的改变可显著改变基因表达水平,这可能与疾病的发生和进展有关。我们推测,肠道组织中细胞因子信号传导抑制因子3基因启动子区域的DNA甲基化状态改变可能与克罗恩病(CD)的易感性有关。

方法

采用实时定量多重甲基化特异性PCR(QM-MSP)检测方法,对15例CD患者及15例年龄、性别匹配的健康对照者肠道组织中该人类基因启动子区域的DNA甲基化状态进行分析。

结果

基于甲基化检测数据分析,我们发现CD患者该基因启动子区域的甲基化程度高于健康对照者(CD中未甲基化DNA 健康对照者;0.00048±0.0011 0.07±0.142,p<0.000)。

结论

此处呈现的数据表明,CD患者结肠黏膜中该基因启动子区域CpG岛的异常甲基化与黏膜炎症状态相关,这为甲基化参与炎症过程的起始及CD的发展提供了见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c596/9077662/fd0e14a79e2e/AJMB-14-165-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c596/9077662/de0defc13956/AJMB-14-165-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c596/9077662/fd0e14a79e2e/AJMB-14-165-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c596/9077662/de0defc13956/AJMB-14-165-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c596/9077662/fd0e14a79e2e/AJMB-14-165-g002.jpg

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本文引用的文献

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