Fig. 2: METTL3 counteracts the aggravation of inflammation caused by ADAP deficiency in TLR4-stimulated macrophages.
From: ADAP-METTL3 modulates the inflammatory responses of macrophages via m6A modification of Spry1
A–C PMs isolated from WT and Adap-/- mice were either untreated or treated with the METTL3-specific inhibitor STM2457 (50 μM) for 24 h. Following treatment, cells were either left unstimulated or stimulated with LPS (1 μg/ml) for 6 h. Total RNA was extracted and subjected to RT-qPCR analysis. The mRNA expression levels of TNF-α (A, n = 3), IL-1β (B, n = 4), and IL-6 (C, n = 4) were normalized to Gapdh mRNA expression. D–F WT and ADAP knockdown RAW 264.7 cells were transfected with either control siRNA (si-NC) or METTL3-specific siRNA (si-METTL3) for 24 h, followed by treatment with or without LPS (1 μg/ml, 6 h). Total RNA was extracted, and RT-qPCR analysis was performed to assess the mRNA expression levels of TNF-α (D), IL-1β (E), and IL-6 (F). Relative mRNA levels were normalized to Gapdh mRNA expression. All RT-qPCR data are presented as mean ± SEM. n = 3. P values were determined by a two-way ANOVA with multiple comparison. *P < 0.05, **P < 0.01, and ***P < 0.001.
