N-Methyladenosine (mA) Methylation Is Associated with the Immune Microenvironments in Acute Intracerebral Hemorrhage (ICH).

Researchers have recently found that N-methyladenosine (mA) is a type of internal posttranscriptional modification that is essential in mammalian mRNA. However, the features of mA 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 mA 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 mA modification, and the differentially expressed mA-modified genes were confirmed by MeRIP-qPCR. We found no significant differences in the total mA 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 mA 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 mA-modified genes may influence the immune microenvironments in acute ICH.