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冠心病中 M1 巨噬细胞基因的异常 DNA 甲基化。

Aberrant DNA methylation of M1-macrophage genes in coronary artery disease.

机构信息

Department of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Department of Cardiology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

出版信息

Sci Rep. 2019 Feb 5;9(1):1429. doi: 10.1038/s41598-018-38040-1.

DOI:10.1038/s41598-018-38040-1
PMID:30723273
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6363807/
Abstract

M1 and M2 macrophage balance in atherosclerosis has attracted much interest. Though, it remains unknown how macrophage heterogeneity is regulated. Moreover, the regulation of macrophage polarization and activation also involve DNA methylation. However, it remains ambiguous which genes are under direct regulation by DNA methylation. Our aim was to evaluate the gene-specific promoter DNA methylation status of M1/M2 polarization markers in PBMCs of CAD patients. A case-control study was performed with 25 CAD patients and 25 controls to study the promoter DNA methylation status of STAT1, STAT6, MHC2, IL12b, iNOS, JAK1, JAK2 and SOCS5 using MS-HRM analysis. Our data indicates that there was a clear-cut difference in the pattern of gene-specific promoter DNA methylation of CAD patients in comparison to controls. A significant difference was observed between the percentage methylation of STAT1, IL12b, MHC2, iNOS, JAK1 and JAK2 in CAD patients and control subjects. In conclusion, our data show that MS-HRM assay is a rapid and inexpensive method for qualitatively identifying aberrant gene-specific promoter DNA methylation changes in CAD. Furthermore, we propose that gene-specific promoter DNA methylation based on monocyte/macrophage might aid as diagnostic marker for clinical application or DNA methylation-related drug interventions may offer novel possibilities for atherosclerotic disease management.

摘要

M1 和 M2 巨噬细胞平衡在动脉粥样硬化中引起了广泛关注。然而，巨噬细胞异质性的调节机制仍不清楚。此外，巨噬细胞极化和激活的调节还涉及 DNA 甲基化。但是，哪些基因受 DNA 甲基化的直接调控仍不清楚。我们的目的是评估 CAD 患者 PBMC 中 M1/M2 极化标志物的基因特异性启动子 DNA 甲基化状态。采用病例对照研究，对 25 例 CAD 患者和 25 例对照进行了研究，采用 MS-HRM 分析检测 STAT1、STAT6、MHC2、IL12b、iNOS、JAK1、JAK2 和 SOCS5 的启动子 DNA 甲基化状态。我们的数据表明，与对照组相比，CAD 患者的基因特异性启动子 DNA 甲基化模式存在明显差异。CAD 患者和对照组之间的 STAT1、IL12b、MHC2、iNOS、JAK1 和 JAK2 的甲基化百分比存在显著差异。结论：MS-HRM 分析是一种快速、经济的方法，可定性鉴定 CAD 中异常的基因特异性启动子 DNA 甲基化改变。此外，我们提出基于单核细胞/巨噬细胞的基因特异性启动子 DNA 甲基化可能有助于作为临床应用的诊断标志物，或者 DNA 甲基化相关药物干预可能为动脉粥样硬化疾病的管理提供新的可能性。

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