Zhou Qiao, Long Li, Shi Guixiu, Zhang Jing, Wu Tong, Zhou Bin
Department of Rheumatology, Sichuan Academy of Medical Science & Sichuan Provincial People's Hospital, No. 32 West Section 2, Yihuan Road, Chengdu, Sichuan 610072, China.
Clin Dev Immunol. 2013;2013:524204. doi: 10.1155/2013/524204. Epub 2013 Oct 10.
To analyze the methylation status of miR-124a loci in synovial tissues of rheumatoid arthritis (RA) patients using methylation-specific polymerase chain reaction (MSP).
DNA obtained from the frozen tissue of 7 RA samples, 6 osteoarthritis (OA) samples, and 3 healthy controls were undergoing bisulfite conversion and then analyzed for miR-124a promoter methylation using MSP assay.
miR-124-a1 and miR-124-a2 promoter methylation were both seen in 71.4% of RA samples compared to 16.7% of OA samples. miR-124-a3 promoter methylation was seen in 57.1% of RA samples and 0% of OA samples. All the three loci were unmethylated in 3 healthy controls.
The methylation status of miR-124a seen in this study concurs with that reported in tumor cells, indicating epigenetic dysregulation constituents, a mechanism in the development of rheumatoid arthritis.
采用甲基化特异性聚合酶链反应(MSP)分析类风湿关节炎(RA)患者滑膜组织中miR-124a基因座的甲基化状态。
从7例RA样本、6例骨关节炎(OA)样本和3例健康对照的冷冻组织中提取的DNA进行亚硫酸氢盐转化,然后使用MSP分析法分析miR-124a启动子甲基化情况。
71.4%的RA样本中可见miR-124-a1和miR-124-a2启动子甲基化,而OA样本中这一比例为16.7%。57.1%的RA样本中可见miR-124-a3启动子甲基化,OA样本中这一比例为0%。3例健康对照中所有三个基因座均未甲基化。
本研究中观察到的miR-124a甲基化状态与肿瘤细胞中报道的一致,表明存在表观遗传失调成分,这是类风湿关节炎发病机制之一。