Methylation of tenascin XB mediated by methyltransferase-like 3 can effectively suppress neural injury and cellular apoptosis induced by ischemic stroke

BACKGROUND: Ischemic stroke (IS), a cerebrovascular disorder due to brain vessel blockage, poses a direct life-threatening risk. Tenascin XB (TNXB), a glycoprotein, is key in regulating extracellular matrix structure and signal transduction. This study aims to unveil the mechanism by which TNXB alleviates IS. METHODS: CCK-8 assay; LDH release was measured with an LDH assay kit; and cell apoptosis rate was evaluated by flow cytometry. TNXB mRNA modification sites were predicted using SRAMP website; the N6-methyladenosine (m6A) level of RNA was detected using MeRIP assay; the half-life of TNXB mRNA was assessed by actinomycin D assay. RESULTS: targeting TNXB. CONCLUSIONS: METTL3 stabilizes TNXB expression through m6A methylation modification, thereby alleviating IS-induced cellular damage. This suggests that targeting the METTL3-TNXB axis may represent a potential therapeutic strategy for IS.