Effect of ABCA1 promoter methylation on premature coronary artery disease and its relationship with inflammation.
Effect of ABCA1 promoter methylation on premature coronary artery disease and its relationship with inflammation.
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DOI：
10.1186/s12872-021-01894-x
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发表时间：
2021-02-08
影响因子：
2.1
通讯作者：
Zhao J
中科院分区：
文献类型：
--
作者：
An F;Liu C;Wang X;Li T;Fu H;Bao B;Cong H;Zhao J
ATP结合盒转运体A1（ABCA 1）在高密度脂蛋白（HDL）代谢和胆固醇逆向转运（RCT）中起重要作用，并发挥抗炎作用。ABCA 1基因启动子甲基化水平升高可能导致冠状动脉疾病的进展。因此，本研究调查了ABCA 1启动子甲基化状态与早发性冠状动脉疾病（pCAD）发展中炎症之间的关系。2019年6月至12月，从中国人民武装警察部队特色医学中心招募PCAD患者和健康个体（各n = 90）。使用焦磷酸测序，评估其血液样本中ABCA 1启动子甲基化水平。还常规测量并比较两组之间的血脂、白细胞介素1β（IL-1β）、C反应蛋白（CRP）和循环游离DNA/神经细胞外陷阱（cfDNA/NETs）的血清浓度。P值< 0.05为有统计学意义。pCAD组ABCA 1基因启动子区甲基化水平显著高于对照组（44.24% ± 3.66 vs.36.05% ± 2.99，P < 0.001）。二元Logistic回归分析显示，ABCA 1基因启动子甲基化水平是pCAD发生的独立危险因素（OR = 2.878，95%可信区间：1.802-4.594，P < 0.001）。此外，ABCA 1启动子甲基化水平与HDL水平呈负相关（r =-0.488，P < 0.001），与CRP、cfDNA/NETs和IL-1β水平呈正相关（r = 0.389，0.404，0.385; P < 0.001）。多元回归分析显示血清CRP、IL-1β和cfDNA/NETs水平独立影响ABCA 1启动子甲基化。我们的研究结果表明，ABCA 1启动子的高甲基化水平与低HDL胆固醇水平和pCAD风险增加有关。炎症因子和NET可能通过影响ABCA 1启动子甲基化水平参与pCAD的进展。
ATP-binding cassette transporter A1 (ABCA1) plays a major role in high-density lipoprotein (HDL) metabolism and reverse cholesterol transport (RCT) and exerts anti-inflammatory effects. Increased ABCA1 promoter methylation level may result in the progression of coronary artery disease. Thus, the present study investigated the association between promoter methylation status of ABCA1 and inflammation in the development of premature coronary artery disease (pCAD). PCAD patients and healthy individuals (n = 90 each) were recruited from the Characteristic Medical Center of the Chinese People's Armed Police Force from June to December 2019. Using pyrosequencing, the levels of ABCA1 promoter methylation in their blood samples were evaluated. Serum concentrations of lipids, interleukin 1β (IL-1β), C-reactive protein (CRP), and circulating free DNA/Neutrophil extracellular traps (cfDNA/NETs) were also routinely measured and compared between the two groups. P values < 0.05 were considered statistically significant. The mean ABCA1 promoter methylation levels were significantly higher in the pCAD group than in the control group (44.24% ± 3.66 vs. 36.05% ± 2.99, P < 0.001). Based on binary logistic regression analysis, ABCA1 promoter methylation level was identified as an independent risk factor for pCAD development (odds ratio = 2.878, 95% confidence interval: 1.802–4.594, P < 0.001). Furthermore, ABCA1 promoter methylation levels were negatively correlated with HDL levels (r = − 0.488, P < 0.001) and positively correlated with the levels of CRP, cfDNA/NETs, and IL-1β (r = 0.389, 0.404, 0.385, respectively; P < 0.001). Multiple regression analysis showed that the serum levels of CRP, IL-1β, and cfDNA/NETs independently affect ABCA1 promoter methylation. Our findings indicate that high methylation levels at the ABCA1 promoter are associated with low HDL cholesterol levels and an increased risk of pCAD. Inflammatory factors and NETs may be involved in the progression of pCAD by affecting ABCA1 promoter methylation levels.
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