Fig. 7: Promotion of B10 cell generation by butyrate and HDACi is dependent on ERK and p38 MAPK activity. | Cell Death & Disease

Fig. 7: Promotion of B10 cell generation by butyrate and HDACi is dependent on ERK and p38 MAPK activity.

From: Effects of short-chain fatty acids in inhibiting HDAC and activating p38 MAPK are critical for promoting B10 cell generation and function

Fig. 7

Splenic B cells isolated from C57BL/6J mice were cultured with or without NaBu under the existence of LPS for 2 days and harvested for RNA-seq analysis. A The principal component analysis was performed on total normalized counts before statistical analysis. B, C Potential key pathways involved in the promotion of B10 cell generation by butyrate. DEGs identified as fold change >2 and p value of < 0.05 were used for gene set enrichment analysis (B) and KEGG pathway analysis (C). D Heatmap of the fold change of differentially expressed cytokines, chemokines, and Breg-related surface markers in cells treated with NaBu compared to the control. E–G Protein level evaluated by immunoblot analysis (E, F) and B10 cell frequency detected by flow cytometry (G) in B cells, which were cultured for 48 h in the presence of LPS with or without NaBu (1 mM) or MAPK inhibitors including ERKi (5 μM), p38i (5 μM), and JNIKi (1 μM). The relative protein levels in immunoblots were semi-quantified by the Image J software and the ratio between the level of phosphorylated and total target protein was calculated and visualized as bar graphs in (F). The data are presented as mean ± SD from three independent experiments. ****P < 0.0001 compared to NaBu.

Back to article page