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趋化因子CXCL14在SLE患者外周血单个核细胞中的表达及启动子甲基化分析

ISSN号：1000-6834
期刊名称：《中国应用生理学杂志》
时间：0
分类：R392.6[医药卫生—免疫学;医药卫生—基础医学]
作者机构：[1]温州医科大学检验医学院、生命科学院,浙江温州325035, [2]温州医科大学第二临床医学院,浙江温州325035, [3]温州医科大学微生物学和免疫学教研室,分子病毒与疫苗研究所,热带医学研究所,浙江温州325035, [4]金华市中医医院检验科,浙江金华321017, [5]金华职业技术学院医学院,浙江金华321017
相关基金：浙江省科技厅科研基金资助项目（2012C33126）; 浙江省大学生新苗计划（2014R413058,2015R413027,2015R413069）; 金华市科技局科研基金资助项目（2013-3-014）

作者：王金丹[1], 黄茜茜[2], 叶璐璐[3], 范超凡[2], 郭刚强[3], 徐玲娟[4], 薛向阳[3], 盛秀胜[5]

关键词：系统性红斑狼疮, 趋化因子, CXCL14, 甲基化, systemic lupus erythematosus（SEE） , chemokine, CXCL14, methylation

中文摘要：

目的：分析趋化因子CXCL14在系统性红斑狼疮（SLE）患者外周血单个核细胞（PBMC）中的表达及其启动子甲基化特征。方法：收集28例SLE患者和20名健康人外周血单个核细胞（PBMC）标本,抽提细胞中RNA,逆转录后,以GAPDH为内参,通过定量PCR检测PBMC中CXCL14的表达,统计分析CXCL14表达水平与SLE各种临床资料的相关性,探讨PBMC中CXCL14表达与SLE的关系,通过重亚硫酸盐修饰的全基因组DNA用以BSP测序来明确不同标本中CXCL14启动子中甲基化位点的甲基化率。结果：CXCL14在SLE患者和正常人PBMC中的表达量存在显著差异（P〈0.05）。与健康人PBMC中CXCL14的含量相比较,CXCL14在SLE患者PBMC中表达量显著降低。与进一步CXCL14表达水平与SLE各种临床资料的相关性分析显示,CXCL14表达水平与SSB抗体（干燥综合征B抗体）、蛋白尿及血小板计数相关。与SSB抗体阴性SLE患者比较,SSB抗体阳性患者CXCL14表达水平更低（P〈0.05）;与蛋白尿阴性SLE患者相比,蛋白尿阳性患者CXCL14表达水平更低（P〈0.05）;而血小板升高患者的CXCL14表达水平更高（P〈0.05）。CXCL14表达水平与SLE活动、肾损害指标、抗ds-DNA、C反应蛋白（CRP）、补体C3水平等指标未见显著相关性。CXCL14启动子区甲基化分析显示,SLE患者Cp G岛甲基化明显高于正常对照。结论：PBMC中低表达的CXCL14与SLE发生发展相关,其启动子区Cp G岛过度甲基化是SLE患者CXCL14低表达的重要机制。

英文摘要：

Objective： To analyze the expression and its promoter methylation of chemokine CXC ligand 14 （CXCL14） in peripheral blood mononuclear cells （PBMCs） from patients with systemic lupus erythematosus （SLE）. Methods： The RNAs of PBMCs from 28 SLE patients and 20 healthy controls were isolated and reversely transcribed into cDNAs. Using GAPDH as the internal reference, the levels of CXCL14 expression were detected by real-time polymerase chain reaction （PCR）. The correlation between CXCL14 expression and the clinic pathological features of SLE were further analyzed. DNA methylation was analyzed by bisulfite sequencing PCR （BSP）. Results： Our data indicated that the level of CXCLI4 in the PBMC of SLE patients was statistically lower than that in healthy controls （ P 〈 0.05）. Further analysis showed that CXCLI4 expression was negatively correlated with anti-Sj glen syndrome B antibody（anti-SSB antibody, P 〈 0.01 ）and albuminuria（ P 〈 0.05）. However, CXCL14 expression was not significantly correlated with the indexes of SLE activity, renal damage, the level of anti-ds-DNA antibodies, complement C3 and C-reactive protein. In addition, we further demonstrated that the CXCL14 promoter hypermethylation expression was significant higher than healthy controls. Conclusion： Down-regulated of CXCL14 expression in PBMC maybe involved in the occurrence or development of SLE disease. The loss of CXCL14 expression was regulated by promoter hypermethylation.

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