Fig. 6: FGF15/FGFR4 suppresses H3K18la-driven Irf7 expression and inflammatory responses in septic macrophages via NF2. | Cell Death & Disease

Fig. 6: FGF15/FGFR4 suppresses H3K18la-driven Irf7 expression and inflammatory responses in septic macrophages via NF2.

From: FGF15/FGFR4 signaling suppresses M1 macrophage polarization and multi-organ inflammation in septic mice by inhibiting H3K18 lactylation-driven Irf7 expression through NF2-Hippo activation

Fig. 6

A Venn diagram showing the identification of DEGs between mouse BMDMs subjected to specific treatments by RNA-seq. B Detection of Irf7, Ndrg1, Odc1, and Rsad2 mRNA expression in mouse BMDMs and RAW264.7 macrophages following treatment with vehicle (Control), LPS, or LPS + rFGF15 by qRT-PCR. C Fold changes in H3K18la enrichment at the promoter regions of Irf7, Ndrg1, Odc1, and Rsad2 in mouse BMDMs and RAW264.7 macrophage in response to LPS stimulation by ChIP-qPCR analysis. D Dectection of H3K18la enrichment at the promoter regions of Irf7 in mouse BMDMs following treatment with LPS or LPS + rFGF15 using the CUT&Tag assay. E Fold changes in H3K18la enrichment at the promoter region of Irf7 in mouse BMDMs and RAW264.7 macrophages following treatment with vehicle (Control), LPS, or LPS + rFGF15 by ChIP-qPCR analysis. F Fold changes in H3K18la enrichment at the promoter region of Irf7 in RAW264.7 macrophages overexpressing the wildtype NF2 (NF2-WT) or phospho-null NF2 mutant (NF2-Mut) following treatment with LPS or LPS + rFGF15 by ChIP-qPCR analysis. G Detection of Irf7 mRNA and protein expression in RAW264.7 macrophages overexpressing the wildtype NF2 (NF2-WT) or phospho-null NF2 mutant (NF2-Mut) following treatment with LPS or LPS + rFGF15 by qRT-PCR and western blot analysis. H, I Assessment of M1/M2 polarization (H) and pro- and anti-inflammatory mediator production (I) in wildtype and Irf7-overexpressing mouse RAW264.7 macrophages following treatment with LPS or LPS + rFGF15 by flow cytometry and ELISA. n = 6, *p < 0.05.

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