甲基化
N6-甲基腺苷
基因
DNA甲基化
核糖核酸
生物
免疫系统
RNA甲基化
信使核糖核酸
脑出血
分子生物学
基因表达
细胞生物学
内科学
免疫学
生物化学
医学
甲基转移酶
蛛网膜下腔出血
作者
Hong Yang,Chong Xie,Yifan Wu,Yuan Cheng,Desheng Zhu,Yangtai Guan
标识
DOI:10.1007/s12035-023-03643-x
摘要
Researchers have recently found that N6-methyladenosine (m6A) is a type of internal posttranscriptional modification that is essential in mammalian mRNA. However, the features of m6A RNA methylation in acute intracerebral hemorrhage (ICH) remain unknown. To explore differential methylations and to discover their functions in acute ICH patients, we recruited three acute ICH patients, three healthy controls, and an additional three patients and healthy controls for validation. The m6A methylation levels in blood samples from the two groups were determined by ultrahigh-performance liquid chromatography coupled with triple quadruple mass spectrometry (UPLC-QQQ-MS). Methylated RNA immunoprecipitation sequencing (MeRIP-seq) was employed to identify differences in m6A modification, and the differentially expressed m6A-modified genes were confirmed by MeRIP-qPCR. We found no significant differences in the total m6A levels between the two groups but observed differential methylation peaks. Compared with the control group, the coding genes showing increased methylation following acute ICH were mostly involved in processes connected with osteoclast differentiation, the neurotrophin signaling pathway, and the spliceosome, whereas genes with reduced m6A modification levels after acute ICH were found to be involved in the B-cell and T-cell receptor signaling pathways. These results reveal that differentially m6A-modified genes may influence the immune microenvironments in acute ICH.
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