METTL17-Mediated Inhibition of M1 Macrophage Polarization Alleviates the Progression of Ankylosing Spondylitis.

RNA methylation is involved in the pathogenesis of ankylosing spondylitis (AS). This study aimed to investigate the potentials of METTL17 in AS. mRNA expression was detected using RT-qPCR. RNA methylation was detected using MeRIP assay. Protein expression was detected using western blot. Cell proliferation was detected using EdU assay. Macrophage functions was detected using flow cytometry. METTL17 was upregulated after exposure to LPS. However, METTL17 knockdown promoted inflammatory response. Moreover, METTL17 knockdown promoted M1 macrophage polarization. Mechanically, METTL17 regulate RNA methylation. Mechanically, METTL17 promoted the RNA methylation of STAT1, inhibiting the mRNA and protein stability of STAT1. In summary, METTL17 inhibits inflammatory response and M1 macrophage polarization via mediating the RNA methylation of STAT1. Therefore, targeting METTL17/STAT1 may be a promising strategy for AS.