Medical Genetics Center, School of Medicine, Ningbo University, Ningbo, Zhejiang 315211, China.
Medical Genetics Center, School of Medicine, Ningbo University, Ningbo, Zhejiang 315211, China.
Immunol Lett. 2017 Oct;190:15-19. doi: 10.1016/j.imlet.2017.06.011. Epub 2017 Jul 6.
C-C motif chemokine ligand 2 (CCL2) encodes a chemokine which amplifies and maintains inflammation through chemokine-cytokine networks. Gout is a type of painful inflammation arthritis in response to the deposition of monosodium urate (MSU) crystals in joints. The purpose of this study was to figure out the role of CCL2 promoter methylation in gout.
A quantitative methylation-specific polymerase chain reaction (qMSP) was used to measure CCL2 promoter methylation in 93 gout patients and 101 healthy controls, respectively. All participants were Chinese Han males. The percent of methylated reference (PMR) was used to evaluate methylation level of each sample.
In the current study, we have found that CCL2 promoter methylation was significantly lower in gout than in healthy controls (24.95% versus 42.68%, P<0.001). CCL2 promoter hypermethylation was considered as a risk factor of gout [OR (95% CI)=3.59E-04 (5.67E-06, 0.023), P=1.79E-04]. Receiver operating characteristic (ROC) curve analysis showed there was a significant diagnostic value of CCL2 hypomethylation for gout (AUC=0.763, 95% CI=0.695-0.830, sensitivity=0.644, specificity=0.849).
CCL2 promoter hypomethylation in peripheral blood could be a potential biomarker for the diagnosis of gout in Chinese Han males.
C 型趋化因子配体 2（CCL2）编码一种趋化因子，通过趋化因子-细胞因子网络放大和维持炎症。痛风是一种因单钠尿酸盐（MSU）晶体在关节中沉积而引起的疼痛性炎症性关节炎。本研究旨在探讨 CCL2 启动子甲基化在痛风中的作用。
采用定量甲基化特异性聚合酶链反应（qMSP）分别检测 93 例痛风患者和 101 例健康对照者的 CCL2 启动子甲基化水平。所有参与者均为中国汉族男性。采用甲基化参考百分比（PMR）评估每个样本的甲基化水平。
本研究发现，痛风患者的 CCL2 启动子甲基化水平明显低于健康对照组（24.95%比 42.68%，P<0.001）。CCL2 启动子超甲基化被认为是痛风的危险因素[比值比（95%置信区间）=3.59E-04（5.67E-06，0.023），P=1.79E-04]。受试者工作特征（ROC）曲线分析显示，CCL2 低甲基化对痛风具有显著的诊断价值（AUC=0.763，95%置信区间=0.695-0.830，敏感度=0.644，特异度=0.849）。
外周血 CCL2 启动子低甲基化可能是中国汉族男性痛风诊断的潜在生物标志物。
