METTL3 suppresses neuropathic pain via modulating N6-methyladenosine-dependent primary miR-150 processing.

ABSTRACT: Methyltransferase-like 3 (METTL3)-modulated N6-methyladenosine (m6A) was recently identified as an important epigenetic regulation type during RNA processing and contributes to multiple pathological processes. Neuropathic pain (NP) is induced by a lesion of the somatosensory nervous system, and the detailed pathways by which METTL3/m6A regulated to modulate gene dysregulation and enable NP have remained unclear. Therefore, this study investigated the function of METTL3-mediated m6A methylation on miRNA maturation, and investigated how this regulation contributes to NP progression. A rat model characterized with typical NP was established by a spared nerve-injury (SNI) method. By analyzing the expression levels of METTL3 and m6A methylation, we found that METTL3, along with m6A methylation,

SUBMITTER: Zhang L 

PROVIDER: S-EPMC8873433 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature