HLA-G 基因 5′ UTR 中 CpG 岛的高甲基化会降低免疫性血小板减少症患者的 HLA-G 基因表达量

IF 2.9 4区 医学 Q1 Medicine
Ji Ma, Yunna Ning, Ke Lu, Hui Wang, Ping Li, Lili Feng, Jianing Zhang, Linna Xie, Qiang He
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引用次数: 0

摘要

本研究调查了免疫性血小板减少症(ITP)患者体内 HLA-G 基因 5′ 非翻译区-CpG 岛(5′ UTR)DNA 甲基化对可溶性 HLA-G (sHLA-G)水平的影响,从而揭示了 sHLA-G 在 ITP 中的调控机制。利用包括ITP患者在内的53名参与者组成的队列,采用Sequenom MassARRAY甲基化分析仪分析了HLA-G基因5′UTR的DNA甲基化图谱。结果显示,ITP 患者特定 CpG 位点(CpG3、CpG18、CpG19 和 CpG20.21)的 DNA 甲基化增加。DNA 甲基化与 sHLA-G 表达呈负相关,尤其是在 CpG18 位点。抗 GPIb/IX 抗体患者的 CpG18 甲基化程度较高。年龄和性别与甲基化无明显相关性。这强调了5′UTR高甲基化在影响循环HLA-G水平中的作用,揭示了ITP的发展和潜在的治疗靶点。通过将DNA甲基化与sHLA-G表达联系起来,这加深了人们对ITP的了解,并提出了新的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hyper-Methylation of CpG Island in 5′ UTR of the HLA-G Gene Reduces Its Expression in Individuals with Immune Thrombocytopenia
This study investigated the impact of DNA methylation in the 5′ untranslated region-CpG island (5′ UTR) of the HLA-G gene on soluble HLA-G (sHLA-G) levels in immune thrombocytopenia (ITP) patients, shedding light on sHLA-G’s regulatory mechanisms in ITP. Using a cohort of 53 participants, including ITP patients, DNA methylation profiles in the HLA-G gene’s 5′ UTR were analyzed with Sequenom MassARRAY Methylation Analysis. sHLA-G levels were measured by enzyme-linked immunosorbent assay, and platelet antibodies were assessed using modified MAIPA. Results showed increased DNA methylation at specific CpG sites (CpG3, CpG18, CpG19, and CpG20.21) in ITP patients. A negative correlation between DNA methylation and sHLA-G expression, particularly at CpG18, was found. Patients with Anti-GPIb/IX antibodies had higher CpG18 methylation. Age and gender didn’t correlate significantly with methylation. This underscores 5′ UTR hypermethylation’s role in influencing circulating HLA-G levels, revealing insights into ITP development and potential therapeutic targets. By linking DNA methylation to sHLA-G expression, this advances ITP understanding, suggesting new therapeutic strategies.
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来源期刊
CiteScore
4.30
自引率
17.20%
发文量
145
审稿时长
2.3 months
期刊介绍: Information not localized
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